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1

Khajuria, Annu, and Donald S. Houston. "Induction of monocyte tissue factor expression by homocysteine: a possible mechanism for thrombosis." Blood 96, no. 3 (August 1, 2000): 966–72. http://dx.doi.org/10.1182/blood.v96.3.966.

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Abstract Moderately elevated plasma homocysteine levels are an important independent risk factor for arterial and venous thrombosis and for atherosclerosis. Some investigators have proposed that homocysteine's effects result from oxidant injury to the vascular endothelium or from an alteration in endothelial function. However, homocysteine may have other cellular targets. We now report that homocysteine, at physiologically relevant concentrations, induces the expression of tissue factor by monocytes. In response to homocysteine, monocytes express procoagulant activity in a dose-dependent and a time-dependent manner. This activity is attributable to tissue factor because it was dependent on factor VII and blocked by anti-tissue factor antibodies. Tissue factor mRNA levels were also increased in monocytes after homocysteine treatment. The effect was found to be specific because analogues of homocysteine (homocystine and homocysteine thiolactone) did not mimic homocysteine's activity, nor did other thiol compounds (cysteine, 2-mercaptoethanol, dithiothreitol). On the other hand, methionine, the metabolic precursor of homocysteine, was active though less potent than homocysteine. Catalase and superoxide dismutase (scavengers of H2O2 and O2− Radicals, respectively) were unable to block the expression of tissue factor induced by homocysteine, as was a 5-fold excess of the reducing agent 2-mercaptoethanol. We conclude that the induction of tissue factor expression by circulating monocytes is a plausible mechanism by which homocysteine may induce thrombosis and that a nonspecific redox process is not involved.
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2

Khajuria, Annu, and Donald S. Houston. "Induction of monocyte tissue factor expression by homocysteine: a possible mechanism for thrombosis." Blood 96, no. 3 (August 1, 2000): 966–72. http://dx.doi.org/10.1182/blood.v96.3.966.015k12_966_972.

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Moderately elevated plasma homocysteine levels are an important independent risk factor for arterial and venous thrombosis and for atherosclerosis. Some investigators have proposed that homocysteine's effects result from oxidant injury to the vascular endothelium or from an alteration in endothelial function. However, homocysteine may have other cellular targets. We now report that homocysteine, at physiologically relevant concentrations, induces the expression of tissue factor by monocytes. In response to homocysteine, monocytes express procoagulant activity in a dose-dependent and a time-dependent manner. This activity is attributable to tissue factor because it was dependent on factor VII and blocked by anti-tissue factor antibodies. Tissue factor mRNA levels were also increased in monocytes after homocysteine treatment. The effect was found to be specific because analogues of homocysteine (homocystine and homocysteine thiolactone) did not mimic homocysteine's activity, nor did other thiol compounds (cysteine, 2-mercaptoethanol, dithiothreitol). On the other hand, methionine, the metabolic precursor of homocysteine, was active though less potent than homocysteine. Catalase and superoxide dismutase (scavengers of H2O2 and O2− Radicals, respectively) were unable to block the expression of tissue factor induced by homocysteine, as was a 5-fold excess of the reducing agent 2-mercaptoethanol. We conclude that the induction of tissue factor expression by circulating monocytes is a plausible mechanism by which homocysteine may induce thrombosis and that a nonspecific redox process is not involved.
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3

Zaw, K., M. T. Hasan, B. Bhowmick, P. B. Khanna, and E. A. Freeman. "Homocysteine and stroke." Reviews in Clinical Gerontology 17, no. 1 (February 2007): 33–38. http://dx.doi.org/10.1017/s0959259807002316.

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Interest in homocysteine's role in vascular disease was stimulated by the paper of McCully (1969) in which, based on autopsy evidence of extensive arterial thrombosis in two children with elevated plasma homocysteine concentrations and homocystinuria, he proposed that elevated plasma homocysteine (hyperhomocysteinaemia) can cause atherosclerotic vascular disease. A meta-analysis of subsequent prospective observational studies concluded that elevated homocysteine is indeed a modest independent predictor of ischaemic heart disease and stroke risk in healthy populations with a 25% reduction in serum homocysteine concentration, a reduction of approximately 3 micromol per litre (μmol/l) being associated with a 19% lower risk of stroke (odds ratio, 0.81; 95% confidence interval (CI), 0.69 – 0.95). In the nationally representative sample of US adults, elevated homocysteine concentration was independently associated with an increased likelihood of non-fatal stroke in both black and white adults. In this article, the current concepts relating homocysteine to ischaemic stroke are reviewed.
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4

Lubec, Barbara, Klaus Arbeiter, Harald Hoeger, and Gert Lubec. "Increased Cyclin Dependent Kinase in Aortic Tissue of Rats Fed Homocysteine." Thrombosis and Haemostasis 75, no. 04 (1996): 542–45. http://dx.doi.org/10.1055/s-0038-1650317.

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Summary Background. Hyperhomocyst(e)inemia is strongly associated with occlusive arterial disease. Several mechanisms for the development of vascular lesions have been described. A direct effect of homocysteine on proliferation of smooth muscle cells and collagen expression was proposed recently. These observations led us to examine the effect of homocysteine on cyclin dependent kinase, the starter of mitosis and reflecting proliferation. Methods and results. Thirty Him: OF A rats were divided into three groups. Ten animals were fed for a period of six weeks 50 mg/kg body wt per day homocysteine, ten the same dose of homocysteic acid and ten remained untreated controls. At the end of the experiment we determined aortic cyclin dependent kinase, phosphokinases A and C, aortic homocyst(e)ine and aortic hydroxyproline. Aortic cyclin dependent kinase was significantly (p = 0.0001) elevated in the homocysteine treated group (mean 120 ± 15) compared with the homocysteic acid treated group (mean 71 ± 11) or the untreated group (mean 72 ± 10 fmol/mg aortic tissue). Aortic homocyst(e)ine was significantly higher in homocysteine treated animals (p = 0.0002) strongly correlating with cyclin dependent kinase (r squared = 0.85, p = 0.0001) and with aortic hydroxyproline (r squared = 0.66, p = 0.0001), which in turn was significantly (p = 0.0001) increased in the homocysteine treated group. Phosphokinases A and C determined to rule out nonspecific effects on kinases were not increased by administered homocysteine. Conclusions. Our findings indicate that homocysteine stimulates aortic cyclin dependent kinase with the possible consequence of proliferation of aortic cells. Aortic collagen accumulation could be explained by either the homocysteine-effect on collagen synthesis described in literature, or secondarily, by increased proliferation of collagen producing aortic cells.
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5

Jiang, Xiaohua, Xiao-feng Yang, Eugen Brailoiu, Hieronim Jakubowski, Andrew I. Schafer, William Durante, and Hong Wang. "Regulation of Homocysteine Transport in Vascular Cells." Blood 108, no. 11 (November 16, 2006): 3926. http://dx.doi.org/10.1182/blood.v108.11.3926.3926.

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Abstract Increased levels of plasma homocysteine is an independent risk factor for cardiovascular disease and has cell-type distinct proatherosclerotic effects on vascular cells. In this study, we characterized L- homocysteine transport in cultured human aortic endothelial and aortic smooth muscle cells. L-homocysteine was transported into vascular cells in a time-dependent fashion. L-homocysteine transport activity was about 2-fold higher in aortic smooth muscle cells. In addition, L-homocysteine transport in both cell types was mediated by sodium-dependent and independent carrier systems. Competition studies revealed that the neutral amino acids cysteine, glycine, serine, tyrosine, alanine, leucine, and methionine, and inhibitors of the cysteine transport systems inhibited L-homocysteine uptake in both cell types, but the inhibition was greater in endothelial cells. Eadie-Hofstee plots demonstrated that L-Hcy transport in endothelial cells had a Michaelis constant (Km) of 79mM and a maximum transport velocity (Vmax) of 873 pmol/mg protein/min. In contrast, homocysteine transport in aortic smooth muscle cells had a lower affinity (Km=212mM) but a higher transport capacity (Vmax=4192 pmol/mg protein/min). Interestingly, increases in pH (pH 6.5–8.2) only inhibited L-homocysteine uptake in endothelial cells. Moreover, L-homocysteine transport in endothelial cells was partially inhibited by lysosomal inhibitors. Our studies indicate that L-homocysteine shares transporter systems with cysteine and can be inhibited for transport by multiple neutral amino acids in vascular cells, and that L-homocysteine transport involves lysosomal transport in endothelial cells. The specific lysosomic feature of L-homocystein transport in endothelial cells may contribute to cell type specific growth inhibitory effects and therefore play a role in homocysteine atherogenic potential.
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6

Nieman, Kristin M., Matthew J. Rowling, Timothy A. Garrow, and Kevin L. Schalinske. "Modulation of Methyl Group Metabolism by Streptozotocin-induced Diabetes and All-trans-retinoic Acid." Journal of Biological Chemistry 279, no. 44 (August 30, 2004): 45708–12. http://dx.doi.org/10.1074/jbc.m408664200.

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The hepatic enzyme glycineN-methyltransferase (GNMT) plays a major role in the control of methyl group and homocysteine metabolism. Because disruption of these vital pathways is associated with numerous pathologies, understanding GNMT control is important for evaluating methyl group regulation. Recently, gluconeogenic conditions have been shown to modulate homocysteine metabolism and treatment with glucocorticoids and/or all-trans-retinoic acid (RA)-induced active GNMT protein, thereby leading to methyl group loss. This study was conducted to determine the effect of diabetes, alone and in combination with RA, on GNMT regulation. Diabetes and RA increased GNMT activity 87 and 148%, respectively. Moreover, the induction of GNMT activity by diabetes and RA was reflected in its abundance. Cell culture studies demonstrated that pretreatment with insulin prevented GNMT induction by both RA and dexamethasone. There was a significant decline in homocysteine concentrations in diabetic rats, owing in part to a 38% increase in the abundance of the transsulfuration enzyme cystathionine β-synthase; treatment of diabetic rats with RA prevented cystathionine β-synthase induction. A diabetic state also increased the activity of the folate-independent homocysteine remethylation enzyme betaine-homocysteineS-methyltransferase, whereas the activity of the folate-dependent enzyme methionine synthase was diminished 52%. In contrast, RA treatment attenuated the streptozotocin-mediated increase in betaine-homocysteineS-methyltransferase, whereas methionine synthase activity remained diminished. These results indicate that both a diabetic condition and RA treatment have marked effects on the metabolism of methyl groups and homocysteine, a finding that may have significant implications for diabetics and their potential sensitivity to retinoids.
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7

Yilmaz, Vural Taner, Erkan Coban, Ali Berkant Avci, Fatih Yilmaz, and Ramazan Cetinkaya. "Levels of Plasma Homocysteine in Obese Women Subjects Homocysteine and Obesity." Turkish Nephrology Dialysis Transplantation 23, no. 2 (May 6, 2014): 91–94. http://dx.doi.org/10.5262/tndt.2014.1002.03.

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8

Razygraev, A. V. "Homocysteine peroxidase activity in rat blood plasma: stoichiometry and enzymatic character of the reaction." Biomeditsinskaya Khimiya 59, no. 6 (2013): 636–43. http://dx.doi.org/10.18097/pbmc20135906636.

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Recently it was shown that the presence of rat blood plasma (as well as of erythrocyte hemolysate) in the reaction mixture containing 43 mM Tris-HCl-buffer (pH 8.5), 0.29 mM EDTA, 19.2 mM sodium azide, 1 mM DL-homocysteine (Hcy), and 198 mM hydrogen peroxide (incubation at 37°C) results in a significant acceleration of the decrease in Hcy concentration caused by addition of H O . In this paper, we present data indicating that the observed activity is the homocysteine:H O -oxidoreductase (homocysteine peroxidase) activity. It has been found that the level of H O -dependent Hcy decrease observed in the presence of blood plasma corresponds to homocysteine:H O -oxidoreductase reaction stoichiometry of 2:1 (mole ratio). The activity observed belongs to the protein fraction isolated by saturation with ammonium sulfate to 50%; the specific activity in this protein fraction is significantly higher than that in the whole plasma. The results confirm the hypothesis that the reaction between Hcy and H O at the presence of plasma is catalyzed by the protein component of plasma and this is the homocysteine peroxidase reaction. This activity is not associated with serum albumin, which is known to function as thiol peroxidase, and probably belongs to extracellular glutathione peroxidase (Gpx3).
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9

Leung, Sin Bond, Huina Zhang, Chi Wai Lau, Yu Huang, and Zhixiu Lin. "Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/679635.

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Hyperhomocysteinemia is associated with an increased risk for cardiovascular diseases through increased oxidative stress. Salidroside is an active ingredient of the root ofRhodiola roseawith documented antioxidative, antihypoxia and neuroprotective properties. However, the vascular benefits of salidroside against endothelial dysfunction have yet to be explored. The present study, therefore, aimed to investigate the protective effect of salidroside on homocysteine-induced endothelial dysfunction. Functional studies on the rat aortas were performed to delineate the vascular effect of salidroside. DHE imaging was used to evaluate the reactive oxygen species (ROS) level in aortic wall and endothelial cells. Western blotting was performed to assess the protein expression associated with oxidative stress and nitric oxide (NO) bioavailability. Exposure to homocysteine attenuated endothelium-dependent relaxations in rat aortas while salidroside pretreatment rescued it. Salidroside inhibited homocystein-induced elevation in the NOX2 expression and ROS overproduction in both aortas and cultured endothelial cells and increased phosphorylation of eNOS which was diminished by homocysteine. The present study shows that salidroside is effective in preserving the NO bioavailability and thus protects against homocysteine-induced impairment of endothelium-dependent relaxations, largely through inhibiting the NOX2 expression and ROS production. Our results indicate a therapeutic potential of salidroside in the management of oxidative-stress-associated cardiovascular dysfunction.
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10

Szegedi, Sandra S., Carmen C. Castro, Markos Koutmos, and Timothy A. Garrow. "Betaine-HomocysteineS-Methyltransferase-2 Is anS-Methylmethionine-Homocysteine Methyltransferase." Journal of Biological Chemistry 283, no. 14 (January 29, 2008): 8939–45. http://dx.doi.org/10.1074/jbc.m710449200.

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11

Wang, Wen-Ming, and Hong-Zhong Jin. "Homocysteine." Chinese Medical Journal 130, no. 16 (August 2017): 1980–86. http://dx.doi.org/10.4103/0366-6999.211895.

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12

SCOTT, CRAIG H., and MARTIN ST JOHN SUTTON. "Homocysteine." Cardiology in Review 7, no. 2 (March 1999): 101–7. http://dx.doi.org/10.1097/00045415-199903000-00013.

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13

Spence, J. David. "Homocysteine." Stroke 37, no. 2 (February 2006): 282–83. http://dx.doi.org/10.1161/01.str.0000199621.28234.e2.

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14

Reeder, Sara Jones, Rosemary L. Hoffmann, Kathy S. Magdic, and Jane M. Rodgers. "Homocysteine." Dimensions of Critical Care Nursing 19, no. 1 (January 2000): 22–28. http://dx.doi.org/10.1097/00003465-200019010-00006.

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15

Abdel-Razik, Ahmed, Waleed Eldars, Rania Elhelaly, Ahmed A. Eldeeb, Mostafa Abdelsalam, Niveen El-Wakeel, and Alsaid Aboulmagd. "Homocysteine." European Journal of Gastroenterology & Hepatology 30, no. 7 (July 2018): 779–85. http://dx.doi.org/10.1097/meg.0000000000001109.

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16

Kraja, Bledar, Adriana Babameto, and Genc Burazeri. "Homocysteine." European Journal of Gastroenterology & Hepatology 30, no. 8 (August 2018): 902–3. http://dx.doi.org/10.1097/meg.0000000000001142.

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17

Langman, Loralie J., and David E. C. Cole. "Homocysteine." Critical Reviews in Clinical Laboratory Sciences 36, no. 4 (January 1999): 365–406. http://dx.doi.org/10.1080/10408369991239231.

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18

Finkelstein, James D., and John J. Martin. "Homocysteine." International Journal of Biochemistry & Cell Biology 32, no. 4 (April 2000): 385–89. http://dx.doi.org/10.1016/s1357-2725(99)00138-7.

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19

Hasty, Robert, and Edward N. Smolar. "Homocysteine." Comprehensive Therapy 28, no. 1 (March 2002): 34–38. http://dx.doi.org/10.1007/s12019-002-0040-x.

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20

Maron, Bradley A., and Joseph Loscalzo. "Homocysteine." Clinics in Laboratory Medicine 26, no. 3 (September 2006): 591–609. http://dx.doi.org/10.1016/j.cll.2006.06.008.

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21

Franklin, Barry. "Homocysteine." ACSM'S Health & Fitness Journal 4, no. 2 (July 1998): 43???44. http://dx.doi.org/10.1249/00135124-199807000-00014.

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22

Popovic, Dragana, Katarina Lalic, Aleksandra Jotic, Tanja Milicic, Jelena Bogdanovic, Maja Đorđevic, Sanja Stankovic, Veljko Jeremic, and Nebojsa M. Lalic. "The inflammatory and hemostatic cardiovascular risk markers during acute hyperglycemic crisis in type 1 and type 2 diabetes." Journal of Medical Biochemistry 38, no. 2 (March 3, 2019): 126–33. http://dx.doi.org/10.2478/jomb-2018-0024.

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Summary Background We analyzed cardiovascular inflammatory (C-reactive protein (CRP), interleukin 6 (IL-6)), haemostatic (homocysteine) risk markers in lean and obese patients at admission and acute hyperglicemic crisis (AHC) resolving, involving diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Methods In that context, we included group A: N = 20 obese, B: N=20 lean patients with DKA; C: N = l0 obese, D: N=10 lean patients with HHS; E: N = 15 obese, F: N=15 lean controls. CRP IL-6, homocysteine were determined by ELISA. Results Our results showed that CRP IL-6, and homocysteine levels decreased in all groups: (A: p<0.001; B: p<0.001, C: p<0.05; D: p<0.001 mg/L), (A: p<0.001 B: p<0.001, C: p<0.001, D: p<0.01 pg/mL), (A: p<0.001, B: p <0.001; C: p<0.05, D: p=0.001 μmol/L), respectively, at resolving AHC. However, CRP persisted higher (p<0.001, p<0.01), IL-6 lower (p<0.05, p<0.001), while homocysteine levels turned out to be similar to controls. Conclusions AHC is associated with increased inflammatory and hemostatic cardiovascular risk markers. Also, insulin therapy in AHC has had more pronounced favorable effect on IL-6 and homocystein than on CRP
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23

Rahman, Aminur, Ratan Das Gupta, Firoz Ahmed Quraishi, Uttam Kumar Saha, Md Nurul Amin Miah, and Zahed Ali. "Relationship Between Homocysteine and Ischemic Stroke." Bangladesh Journal of Medicine 25, no. 1 (September 20, 2015): 8–12. http://dx.doi.org/10.3329/bjmed.v25i1.25071.

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Background: Epidemiologic studies have identified hyper-homocysteinemia as a possible risk factor for atherosclerosis. The aim of the study was based on evaluation of relationship between homocysteinemia with ischemic stroke patients.Methods and materials: It was a prospective observational study conducted in the Department of Neurology, Sir Salimullah Medical College & Mitford hospital, Dhaka. Thirty six consecutive patients with ischemic stroke were analyzed by serum total homocysteine, total cholesterol, HDLcholesterol, LDL-cholesterol, triglyceride and Equal number of of controls same ages were compared with the case group.Result: Mean Fasting blood sugar, serum fasting total cholesterol (TC), serum fasting Low density lipoprotein (LDL) were significantly higher in case group (p=0.001). Serum TC and LDL had a positive correlation with serum homocystine a (p=0.001). Serum High density lipoprotein (HDL) had a negative correlation (p=0.718) and serum triglyceride (TG) had a negative correlation (p = 0.182). Total plasma fasting homocysteine level in case group was 21.89 ± 9.38 ìmol/l and control group was 12.31 ± 3.27 ìmol/l, (p=0.001). Elevated fasting homocystein level was found in 75.0% of ischemic stroke patient and in 16.67% of healthy controls (p=0.001). The incidence of hyperhomocysteinemia is higher in ischaemic stroke cases than that in age-sex matched healthy controls. Hyperhomocysteinemia in ischaemic stroke patients has as been determined as vascular risk factor in our study. Significant correlation has been found between homocysteine concentration and ischaemic stroke.Bangladesh J Medicine Jan 2014; 25 (1) : 8-12
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24

Rahman, Aminur, Ratan Das Gupta, Firoz Ahmed Quraishi, Uttam Kumar Saha, Md Nurul Amin Miah, and Zahed Ali. "Relationship Between Homocysteine and Ischemic Stroke." Journal of Medicine 14, no. 1 (April 12, 2013): 47–51. http://dx.doi.org/10.3329/jom.v14i1.14536.

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Background: Epidemiologic studies have identified hyper-homocysteinemia as a possible risk factor for atherosclerosis.The aim of my study was based on evaluation of relationship between homocysteinemia with ischemic stroke patients. Methods and materials: It was a prospective observational study conducted in the Department of Neurology, Sir Salimullah Medical College & Mitford hospital, Dhaka. Thirty six consecutive patients with ischemic stroke were analyzed by serum total homocysteine, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride and Equal number of controls same ages were compared with the case group. Result: Mean Fasting blood sugar, serum fasting total cholesterol (TC), serum fasting Low density lipoprotein (LDL) were significantly higher in case group (p=0.001). Serum TC and LDL had a positive correlation with serum homocystine a (p=0.001). Serum High density lipoprotein (HDL) had a negative correlation (p=0.718) and serum triglyceride (TG) had a negative correlation (p = 0.182). Total plasma fasting homocysteine level in case group was 21.89 ± 9.38 ìmol/l and control group was 12.31 ± 3.27 ìmol/l, (p=0.001). Elevated fasting homocystein level was found in 75.0% of ischemic stroke patient and in 16.67% of healthy controls (p=0.001). The incidence of hyperhomocysteinemia is higher in ischaemic stroke cases than that in age-sex matched healthy controls. Conclusion: Hyperhomocysteinemia in ischaemic stroke patients has as been determined as vascular risk factor in our study. Significant correlation has been found between homocysteine concentration and ischaemic stroke.DOI: http://dx.doi.org/10.3329/jom.v14i1.14536 J MEDICINE 2013; 14 : 47-51
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25

Markovsky, Aleksandr V. "ADDITIVE EFFECT OF GENES POLYMORPHISM OF FOLATE CYCLE PROTEINS AND HOMOCYSTEIN LEVEL IN PATIENTS WITH PROLIFERATIVE DISEASES OF THE BREAST AS A POTENTIAL FACTOR OF THE RISK OF THROMBOSSES." Atherothrombosis Journal, no. 2 (December 27, 2018): 46–53. http://dx.doi.org/10.21518/2307-1109-2018-2-46-53.

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Aim.The aim of study was to examine the relationship between serum and mammary gland homocysteine levels with the carrier of separate SNP (single nucleotide polymorphism) genes of the folate metabolism system in patients with proliferative diseases and breast cancer.Methods and results.The study included 182 patients with proliferative diseases of the mammary gland in transbaikalia. The control group included 144 women who did not have oncological diseases. The serum homocysteine level and the supernatant of the mammary tissue homogenate were evaluated by high performance liquid chromatography. Genotyping for the detection of polymorphism MTHFRС677T, MTHFRА1298C, MTRA2756G, MTRRA66G was carried out by polymerase chain reaction with the detection of the amplification product in real time. In the course of molecular genetic testing in patients with proliferative diseases of the mammary gland, there was found: 1) the absence of an explicit association of the carriage of genetic polymorphism MTHFRС677T, MTHFRА1298C, MTRA2756G and MTRRA66G with serum homocysteine concentration, however, comparative hyperhomocysteinemia and, to a lesser extent, in women with the benign breast diseases; 2) the highest homocysteine content in the blood in patients with breast cancer whose genotype was characterized by combinations of polymorphic alleles MTR2756G x MTRR66G; 3) that the MTR2756A allele and genotype MTHFR1298AC, especially their combination of MTHFR1298AC x MTR2756A, increase the risk of developing benign breast formations; 4) the effect of the risk alleles MTR2756G and MTRR66GON the concentration of homocystein in the tumor tissue of the mammary gland.Conclusion. These patterns indicate a certain contribution of the polymorphisms studied, especially their additive effect, both in the development of proliferative diseases of the mammary gland and in the possible potentiation of prothrombotic effects in these patients against the background of tumor progression and homocysteine metabolism disorders.
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26

HASHMI, SYED FASIH AHMED, MASHOOQ ALI DASTI, MUKHTIAR HUSSAIN JAFFERY, and Syed Zulfiquar Ali Shah. "SERUM HOMOCYSTEINE;." Professional Medical Journal 20, no. 06 (December 15, 2013): 932–37. http://dx.doi.org/10.29309/tpmj/2013.20.06.1567.

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objective: To evaluate the serum homocysteine level in patients with hypertension at Liaquat University HospitalHyderabad. Patients and methods: This six months study was conducted at Liaquat University Hospital Hyderabad. All the hypertensivepatients for ≥ 01 years duration, of ≥ 35 years of age and either gender visited at the cardiac logy OPD or admitted incardiac ward were registered and evaluated for their homocysteine level. The normal plasma homocysteine level isbetween 5 to <15 μmol/L. The results of plasma homocysteine level were interpreted as normal, moderate,intermediate and severe according to the reference range (moderate = 15 to 30 μmol/L; intermediate = 30 to 100μmol/L; severe = >100 μmol/L). The frequency and percentage was calculated for hyperhomocysteinemia in hypertensivepatients. The chi-square and independent t-test was applied between categorical variables at 95% confidence interval and the p-value ≤0.05 was considered as statistically significant. Results: Total 120 hypertensive patients were registered for study. Of these 86(71.7%)were males and 34 (28.3%) were female. Regarding plasma homocysteine level, hyperhomocysteinemia was observed in 99(83%)hypertensive patients, of which 75(75.8%) were males and 24(24.2%) were females while the 21(17.5%) subjects hadnormohomocysteinemia [p=0.04]. According to the categorical classification of plasma homocysteine level, the moderate wasidentified in 58(48%), intermediate in 19 (16%) and severe in 22 (18%) [p = 0.04]. The mean systolic and diastolic blood pressure inoverall population was 160 ± 26 and 90 ± 16 [p=0.02] respectively. The mean ± SD for plasma homocysteine level in overallpopulation was 72.83 ± 12.61 whereas the mean ±SD of patients with normal, moderate, intermediate and severe plasmahomocysteine level was 7.1 ± 1.8, 21±2.7, 60±12.4 and 116 ±7.3 respectively. Conclusion: It is observed that serum homocysteineappears to be raised in patients with hypertension. The hyperhomocysteinemia may be involved in the induction and sustaining of
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27

Elliott, Kathleen M. "Homocysteine testing." Critical Care Nurse 23, no. 2 (April 1, 2003): 21. http://dx.doi.org/10.4037/ccn2003.23.2.21-a.

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28

Selhub, J. "HOMOCYSTEINE METABOLISM." Annual Review of Nutrition 19, no. 1 (July 1999): 217–46. http://dx.doi.org/10.1146/annurev.nutr.19.1.217.

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29

HASHIMOTO, Takao, Yoshihiko SHINOHARA, and Hiroshi HASEGAWA. "Homocysteine Metabolism." YAKUGAKU ZASSHI 127, no. 10 (October 1, 2007): 1579–92. http://dx.doi.org/10.1248/yakushi.127.1579.

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30

Kalantar-Zadeh, K., C. Block, and J. D. Kopple. "PLASMA HOMOCYSTEINE." ASAIO Journal 49, no. 2 (March 2003): 199. http://dx.doi.org/10.1097/00002480-200303000-00234.

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31

Makhro, A. V., E. R. Bulygina, and A. A. Boldyrev. "Effects of homocysteine and homocysteinic acid on cerebellar granule cells." Neurochemical Journal 1, no. 2 (June 2007): 127–32. http://dx.doi.org/10.1134/s1819712407020031.

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32

Miller, Danielle, Huimin Xu, and Robert H. White. "S-Inosyl-l-Homocysteine Hydrolase, a Novel Enzyme Involved inS-Adenosyl-l-Methionine Recycling." Journal of Bacteriology 197, no. 14 (April 27, 2015): 2284–91. http://dx.doi.org/10.1128/jb.00080-15.

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ABSTRACTS-Adenosyl-l-homocysteine, the product ofS-adenosyl-l-methionine (SAM) methyltransferases, is known to be a strong feedback inhibitor of these enzymes. A hydrolase specific forS-adenosyl-l-homocysteine producesl-homocysteine, which is remethylated to methionine and can be used to regenerate SAM. Here, we show that the annotatedS-adenosyl-l-homocysteine hydrolase inMethanocaldococcus jannaschiiis specific for the hydrolysis and synthesis ofS-inosyl-l-homocysteine, notS-adenosyl-l-homocysteine. This is the first report of an enzyme specific forS-inosyl-l-homocysteine. As withS-adenosyl-l-homocysteine hydrolase, which shares greater than 45% sequence identity with theM. jannaschiihomologue, theM. jannaschiienzyme was found to copurify with bound NAD+and hasKmvalues of 0.64 ± 0.4 mM, 0.0054 ± 0.006 mM, and 0.22 ± 0.11 mM for inosine,l-homocysteine, andS-inosyl-l-homocysteine, respectively. No enzymatic activity was detected withS-adenosyl-l-homocysteine as the substrate in either the synthesis or hydrolysis direction. These results prompted us to redesignate theM. jannaschiienzyme anS-inosyl-l-homocysteine hydrolase (SIHH). Identification of SIHH demonstrates a modified pathway in this methanogen for the regeneration of SAM fromS-adenosyl-l-homocysteine that uses the deamination ofS-adenosyl-l-homocysteine to formS-inosyl-l-homocysteine.IMPORTANCEIn strictly anaerobic methanogenic archaea, such asMethanocaldococcus jannaschii, canonical metabolic pathways are often not present, and instead, unique pathways that are deeply rooted on the phylogenetic tree are utilized by the organisms. Here, we discuss the recycling pathway forS-adenosyl-l-homocysteine, produced fromS-adenosyl-l-methionine (SAM)-dependent methylation reactions, which uses a hydrolase specific forS-inosyl-l-homocysteine, an uncommon metabolite. Identification of the pathways and the enzymes involved in the unique pathways in the methanogens will provide insight into the biochemical reactions that were occurring when life originated.
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33

Yang, Qin, and Guo-Wei He. "Imbalance of Homocysteine and H2S: Significance, Mechanisms, and Therapeutic Promise in Vascular Injury." Oxidative Medicine and Cellular Longevity 2019 (November 22, 2019): 1–11. http://dx.doi.org/10.1155/2019/7629673.

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While the role of hyperhomocysteinemia in cardiovascular pathogenesis continuously draws attention, deficiency of hydrogen sulfide (H2S) has been growingly implicated in cardiovascular diseases. Generation of H2S is closely associated with the metabolism of homocysteine via key enzymes such as cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE). The level of homocysteine and H2S is regulated by each other. Metabolic switch in the activity of CBS and CSE may occur with a resultant operating preference change of these enzymes in homocysteine and H2S metabolism. This paper presented an overview regarding (1) linkage between the metabolism of homocysteine and H2S, (2) mutual regulation of homocysteine and H2S, (3) imbalance of homocysteine and H2S in cardiovascular disorders, (4) mechanisms underlying the protective effect of H2S against homocysteine-induced vascular injury, and (5) the current status of homocysteine-lowering and H2S-based therapies for cardiovascular disease. The metabolic imbalance of homocysteine and H2S renders H2S/homocysteine ratio a potentially reliable biomarker for cardiovascular disease and development of drugs or interventions targeting the interplay between homocysteine and H2S to maintain the endogenous balance of these two molecules may hold an even bigger promise for management of vascular disorders than targeting homocysteine or H2S alone.
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34

Alloli, Deepa, G. S. Mahishale, Siddaraya Hanjagi, Sayed Mohammed Meraj Hussaini, and Ganga Patil. "Plasma homocysteine levels in Indian patients with acute ischemic stroke." International Journal of Research in Medical Sciences 6, no. 11 (October 25, 2018): 3684. http://dx.doi.org/10.18203/2320-6012.ijrms20184430.

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Background: Homocysteine has primary atherogenic and prothrombotic properties. The present study aimed to assess serum homocysteine levels in patients with ischemic stroke and to find association of serum homocysteine levels with various patient related variables.Methods: This observational study included patients who were admitted with the diagnosis of stroke in Sri Ventateswara Ramnarain Ruia Government General Hospital. Patients were evaluated for risk factors like hypertension, diabetes mellitus and hyperlipidemia. Total homocysteine estimation was done and survival of the patients was assessed at the time of discharge from the hospital.Results: Most common risk factor for stroke in our study population was dyslipidemia (40%), followed by hypertension (36%). Total homocysteine levels were raised in 92% of the patients. Patients with homocysteine levels less than 15mM/L had lacunar infarcts. Homocysteine levels higher than 100mM/L were found in 18% of the patients and they all had large sized lesions. Significantly higher mean homocysteine levels were found among patients with large lesions (70.15±2.65 vs 21.68±8.02, p value <0.05). Among various risk factors, higher mean homocysteine levels were found to be associated with dyslipidemia (p value <0.05). No association between hypertension, diabetes mellitus or smoking history was found with higher homocysteine levels. Patients who survived had significantly lower homocysteine levels as compared to non survivors (39.3±19.84 vs 100±18.82, p value<0.001).Conclusions: Further studies are needed on homocysteine and stroke fur using homocysteine as screening test and for initiation of preventive therapy of stroke based on homocysteine levels.
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35

McKinley, Michelle C. "Nutritional aspects and possible pathological mechanisms of hyperhomocysteinaemia: an independent risk factor for vascular disease." Proceedings of the Nutrition Society 59, no. 2 (May 2000): 221–37. http://dx.doi.org/10.1017/s0029665100000252.

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Numerous case–control and prospective studies have identified elevated plasma homocysteine as a strong independent risk factor for cerebovascular, cardiovascular and peripheral vascular disease. Homocysteine is formed as a result of the breakdown of the dietary amino acid methionine. Once formed, homocysteine is either remethylated to methionine, or undergoes a trans-sulfuration reaction to form cysteine. The re-methylation of homocysteine to methionine is dependent on three B-vitamins, i.e. riboflavin, vitamin B12and folate. The second pathway of homocysteine metabolism is the trans-sulfuration pathway which requires both vitamin B6and riboflavin for its activity. Thus, up to four B-vitamins are required for intracellular homocysteine metabolism. Many studies have noted strong inverse relationships between homocysteine levels and the status of both vitamin B12and folate. However, the relationship between vitamin B6status and homocysteine is still uncertain. Similarly, numerous intervention studies have demonstrated effective lowering of homocysteine levels as a result of folate and vitamin B12supplementation, while the homocysteine-lowering ability of vitamin B6is unclear. Even though riboflavin plays a crucial role in both the trans-sulfuration and remethylation pathways of homocysteine metabolism, the relationship between riboflavin status and homocysteine levels has not been investigated. The exact mechanism that explains the vascular toxicity of elevated homocysteine levels is unknown at present, studies indicate that it is both atherogenic and thrombogenic. To date, no randomized clinical trial has demonstrated that lowering of homocysteine levels is beneficial in terms of reducing the prevalence of vascular disease. It is probable, however, that optimal B-vitamin status is important in the prevention of vascular disease.
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36

Mansoor, M. A., A. B. Guttormsen, T. Fiskerstrand, H. Refsum, P. M. Ueland, and A. M. Svardal. "Redox status and protein binding of plasma aminothiols during the transient hyperhomocysteinemia that follows homocysteine administration." Clinical Chemistry 39, no. 6 (June 1, 1993): 980–85. http://dx.doi.org/10.1093/clinchem/39.6.980.

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Abstract We administered reduced L-homocysteine perorally (67 mumol/kg of body wt) to 12 healthy subjects and injected the same dose into one person, and determined the kinetics of the alterations in reduced, oxidized, and protein-bound concentrations of homocysteine, cysteine, and cysteinylglycine. After oral intake, reduced homocysteine increased rapidly (tmax &lt; or = 15 min), reaching concentrations [3.97 (SD 2.99) mumol/L] 20-fold above fasting values, and then declined towards the normal concentration within 2 h. There was a similar increase in reduced cysteine and a moderate increase in reduced cysteinylglycine. During this response, we observed a positive correlation between the reduced/total ratio for homocysteine and cysteine. When homocysteine was injected, the increase in reduced homocysteine preceded the increase in reduced cysteine by about 3 min. After oral loading, oxidized homocysteine showed a transient increase (tmax = 30 min) that lagged behind the increase of reduced homocysteine. Oxidized cysteine and cysteinylglycine were stable or decreased slightly. Protein-bound homocysteine increased the least rapidly after homocysteine administration (tmax = 1-2 h), and returned to normal values slowly. Changes in protein-bound homocysteine essentially mirrored a concurrent decrease in protein-bound cysteine, suggesting displacement of bound cysteine. These data show that plasma homocysteine has a pronounced, direct effect on the redox status and protein binding of other plasma thiol components. Such effects should be recognized when studying the mechanisms behind the atherogenic effect of increased plasma homocysteine.
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37

Frauscher, G., E. Karnaukhova, A. Muehl, H. Hoeger, and B. Lubec. "Oral administration of homocysteine leads to increased plasma triglycerides and homocysteic acid — additional mechanisms in homocysteine induced endothelial damage?" Life Sciences 57, no. 8 (July 1995): 813–17. http://dx.doi.org/10.1016/0024-3205(95)02009-8.

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38

Jiracek, Jiri, Michaela Collinsova, Ivan Rosenberg, Milos Budesinsky, Eva Protivinska, Hana Netusilova, and Timothy A. Garrow. "S-Alkylated Homocysteine Derivatives: New Inhibitors of Human Betaine-HomocysteineS-Methyltransferase." Journal of Medicinal Chemistry 49, no. 13 (June 2006): 3982–89. http://dx.doi.org/10.1021/jm050885v.

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39

Joubert, Lanae M., and Melinda M. Manore. "Exercise, Nutrition, and Homocysteine." International Journal of Sport Nutrition and Exercise Metabolism 16, no. 4 (August 2006): 341–61. http://dx.doi.org/10.1123/ijsnem.16.4.341.

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Homocysteine is an independent cardiovascular disease (CVD) risk factor modi-fable by nutrition and possibly exercise. While individuals participating in regular physical activity can modify CVD risk factors, such as total blood cholesterol levels, the impact physical activity has on blood homocysteine concentrations is unclear. This review examines the influence of nutrition and exercise on blood homocysteine levels, the mechanisms of how physical activity may alter homocys-teine levels, the role of homocysteine in CVD, evidence to support homocysteine as an independent risk factor for CVD, mechanisms of how homocysteine increases CVD risk, and cut-off values for homocysteinemia. Research examining the impact of physical activity on blood homocysteine levels is equivocal, which is partially due to a lack of control for confounding variables that impact homocysteine. Duration, intensity, and mode of exercise appear to impact blood homocysteine levels differently, and may be dependent on individual fitness levels.
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40

Sengupta, Shantanu, Charles Wehbe, Alana K. Majors, Michael E. Ketterer, Patricia M. DiBello, and Donald W. Jacobsen. "Relative Roles of Albumin and Ceruloplasmin in the Formation of Homocystine, Homocysteine-Cysteine-mixed Disulfide, and Cystine in Circulation." Journal of Biological Chemistry 276, no. 50 (October 9, 2001): 46896–904. http://dx.doi.org/10.1074/jbc.m108451200.

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Disulfide forms of homocysteine account for >98% of total homocysteine in plasma from healthy individuals. We recently reported that homocysteine reacts with albumin-Cys34-S–S-cysteine to form homocysteine-cysteine mixed disulfide and albumin-Cys34thiolate anion. The latter then reacts with homocystine or homocysteine-cysteine mixed disulfide to form albumin-bound homocysteine (Sengupta, S., Chen, H., Togawa, T., DiBello, P. M., Majors, A. K., Büdy, B., Ketterer, M. E., and Jacobsen, D. W. (2001)J. Biol. Chem. 276, 30111–30117). We now extend these studies to show that human albumin, but not ceruloplasmin, mediates the conversion of homocysteine to its low molecular weight disulfide forms (homocystine and homocysteine-cysteine mixed disulfide) by thiol/disulfide exchange reactions. Only a small fraction of homocystine is formed by an oxidative process in which copper bound to albumin, but not ceruloplasmin, mediates the reaction. When copper is removed from albumin by chelation, the overall conversion of homocysteine to its disulfide forms is reduced by only 20%. Ceruloplasmin was an ineffective catalyst of homocysteine oxidation, and immunoprecipitation of ceruloplasmin from human plasma did not inhibit the capacity of plasma to mediate the conversion of homocysteine to its disulfide forms. In contrast, ceruloplasmin was a highly efficient catalyst for the oxidation of cysteine and cysteinylglycine to cystine and bis(-S-cysteinylglycine), respectively. However, when thiols (cysteine and homocysteine) that are disulfide-bonded to albumin-Cys34are removed by treatment with dithiothreitol to form albumin-Cys34–SH (mercaptalbumin), the conversion of homocysteine to its disulfide forms is completely blocked. In conclusion, albumin mediates the formation of disulfide forms of homocysteine by thiol/disulfide exchange, whereas ceruloplasmin converts cysteine to cystine by copper-dependent autooxidation.
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41

Donnelly, James G., and Phillip A. Isotalo. "Non-fasting reference intervals for the Abbott IMxTM homocysteine and AxSYMTM plasma folate assays: influence of the methylenetetrahydrofolate reductase 677 C→T mutation on homocysteine." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 37, no. 3 (May 1, 2000): 390–98. http://dx.doi.org/10.1258/0004563001899339.

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Plasma homocysteine comes under both genetic and nutritional control. B vitamins and particularly folate are important factors in homocysteine metabolism. We have obtained reference intervals for total plasma homocysteine and plasma folate. We have also determined the influence of methylenetetrahydrofolate reductase (MTHFR) genotype on plasma homocysteine concentrations in healthy individuals. Reference intervals for Abbott IMxTM homocysteine and AxSYMTM plasma folate assays were established using 116 volunteers recruited from hospital staff. Exclusion criteria included cardiac, hepatic or renal disorders, and use of over-the-counter prescription medications. An exception was the inclusion of three women using oral contraceptives and one woman receiving post-menopausal oestrogen supplementation. Methylenetetrahydrofolate reductase 677C-T genotyping was performed on 101 of the volunteers to determine whether the MTHFR 677T allele influences homocysteine concentrations in healthy individuals. Reference intervals for homocysteine and folate were determined using the mean±2 standard deviations of the data. Folate/homocysteine ratios were sorted by MTHFR C677T genotype. Homocysteine correlated negatively with plasma folate. Mean male homocysteine concentrations were significantly higher (9· μmol/L; P<0·05) than the mean value (7·1 μmol/L) obtained for females. Mean homocysteine values were significantly higher in subjects who were homozygous for the MTHFR 677T allele when compared with the 677CC genotype ( P<0·05). Ratios of folate/homocysteine were 20% and 7·44% lower in the male and female 677TT group than in the 677CC group, respectively. The mean homocysteine value of 43 volunteers who were taking multivitamins was not significantly different from that of 73 who were not vitamin supplemented. Conversely, the mean folate value was slightly greater, and statistically significant, in the group taking vitamin supplements. The mean folate values and reference intervals were not significantly different when grouped by sex or age. MTHFR 677C T mutations influenced homocysteine values observed in our study of healthy volunteers, even though we did not observe outright folate-deficient individuals. Our random homocysteine values were similar to the fasting homocysteine values obtained in other studies.
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42

Brönstrup, Hages, and Pietrzik. "Lowering of Homocysteine Concentrations in Elderly Men and Women." International Journal for Vitamin and Nutrition Research 69, no. 3 (May 1, 1999): 187–93. http://dx.doi.org/10.1024/0300-9831.69.3.187.

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B-vitamin supplementation has previously been shown to lower the concentration of plasma total homocysteine, a risk factor for cardiovascular disease. Little is known about the homocysteine-lowering effects of low-dose B-vitamins in elderly individuals, who are prone to higher homocysteine levels due to advanced age and a greater frequency of impaired vitamin status. We aimed to identify if and to what extent B-vitamins lower total homocysteine and its subfractions in elderly individuals. Men and women (>= 60 years) received either B-vitamins (400 mug folic acid +1.65 mg pyridoxine +3 mug cyanocobalamin) or a placebo daily for 4 weeks. Subjects in the vitamin group showed a significant decrease in plasma total homocysteine during the first 2 weeks; thereafter, total homocysteine only slightly decreased further resulting in a geometric mean reduction of –16.3% (95% CI: –11.3% to –21.0%) over the entire treatment period. Free homocysteine decreased as well. However, the observed higher ratio of free/total homocysteine after 4 weeks of supplementation suggest a more pronounced reduction in protein-bound homocysteine. Low-dose B-vitamin supplementation is effective in lowering homocysteine in elderly individuals. Further studies are needed to be able to depict the effect of B-vitamin supplementation on different homocysteine subfractions in plasma.
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43

Tessari, Paolo, Edward Kiwanuka, Anna Coracina, Michela Zaramella, Monica Vettore, Anna Valerio, and Giacomo Garibotto. "Insulin in methionine and homocysteine kinetics in healthy humans: plasma vs. intracellular models." American Journal of Physiology-Endocrinology and Metabolism 288, no. 6 (June 2005): E1270—E1276. http://dx.doi.org/10.1152/ajpendo.00383.2004.

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Methionine is a sulfur-containing amino acid that is reversibly converted into homocysteine. Homocysteine is an independent cardiovascular risk factor frequently associated with the insulin resistance syndrome. The effects of insulin on methionine and homocysteine kinetics in vivo are not known. Six middle-aged male volunteers were infused with l-[ methyl-2H3,1-13C]methionine before (for 3 h) and after (for 3 additional hours) an euglycemic hyperinsulinemic (150 mU/l) clamp. Steady-state methionine and homocysteine kinetics were determined using either plasma (i.e., those of methionine) or intracellular (i.e., those of plasma homocysteine) enrichments. By use of plasma enrichments, insulin decreased methionine rate of appearance (Ra; both methyl- and carbon Ra) by 25% ( P < 0.003 vs. basal) and methionine disposal into proteins by 50% ( P < 0.0005), whereas it increased homocysteine clearance by ∼70% ( P < 0.025). With intracellular enrichments, insulin increased all kinetic rates, mainly because homocysteine enrichment decreased by ∼40% ( P < 0.001). In particular, transmethylation increased sixfold ( P < 0.02), transsulfuration fourfold ( P = 0.01), remethylation eightfold ( P < 0.025), and clearance eightfold ( P < 0.004). In summary, 1) physiological hyperinsulinemia stimulated homocysteine metabolic clearance irrespective of the model used; and 2) divergent changes in plasma methionine and homocysteine enrichments were observed after hyperinsulinemia, resulting in different changes in methionine and homocysteine kinetics. In conclusion, insulin increases homocysteine clearance in vivo and may thus prevent homocysteine accumulation in body fluids. Use of plasma homocysteine as a surrogate of intracellular methionine enrichment, after acute perturbations such as insulin infusion, needs to be critically reassessed.
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44

Li, Fang, Gulibositan Aji, Yun Wang, Zhiqiang Lu, and Yan Ling. "Thyroid Peroxidase Antibody is Associated with Plasma Homocysteine Levels in Patients with Graves’ Disease." Experimental and Clinical Endocrinology & Diabetes 128, no. 01 (July 2, 2018): 8–14. http://dx.doi.org/10.1055/a-0643-4692.

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Abstract Purpose Homocysteine is associated with cardiovascular, inflammation and autoimmune diseases. Previous studies have shown that thyroid peroxidase antibody is associated with homocysteine levels in hypothyroidism. The relationship between thyroid antibodies and homocysteine in hyperthyroidism remains unclear. In this study, we aimed to investigate the association of thyroid antibodies with homocysteine in patients with Graves’ disease. Methods This was a cross-sectional study including 478 Graves’ disease patients who were consecutively admitted and underwent radioiodine therapy. Homocysteine, thyroid hormones, thyroid antibodies, glucose and lipids were measured. Results Patients with homocysteine levels above the median were older and had unfavorable metabolic parameters compared to patients with homocysteine levels below the median. Thyroglobulin antibody or thyroid peroxidase antibody was associated with homocysteine levels (β=0.56, 95%CI 0.03-1.08, p=0.04; β=0.75, 95%CI 0.23-1.27, p=0.005). The relationship between thyroid peroxidase antibody and homocysteine remained significant when additionally adjusting for free triiodothyronine (β=0.76, 95%CI 0.24-1.28, p=0.004). The presence of a homocysteine level above the median increased significantly with increasing thyroid peroxidase antibody quartiles in the logistic regression (OR=1.74, 95%CI 1.27-2.39, P for trend=0.001). Homocysteine levels increased significantly with increasing thyroid peroxidase antibody quartiles (p=0.005). Thyroid peroxidase antibody had no significant effect on other traditional cardiovascular risk factors. Conclusions Thyroid peroxidase antibody is independently and positively associated with homocysteine levels in patients with Graves’ disease. Thyroid peroxidase antibody may be associated with the cardiovascular risk of patients with Graves’ disease through its effect on homocysteine.
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45

Shazia Junaid, Sadia Rehman, Hina Moazzam, Iftikhar Yosuf, Lubna Gohar, and Irum Saddiqa. "Association of serum homocysteine with type II diabetic retinopathy." Professional Medical Journal 29, no. 11 (October 31, 2022): 1678–82. http://dx.doi.org/10.29309/tpmj/2022.29.11.7196.

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Objective: To elucidate the association of serum homocysteine with diabetic retinopathy. Study Design: Case Control study. Setting: Department of Physiology and Centre for Research in Experimental and Applied Medicine (CREAM), Army Medical College, in Collaboration with Armed Forces Institute of Ophthalmology, Rawalpindi. Period: December 2019 to December 2020. Material & Methods: A total of ninety subjects were enrolled in the study which were subdivided into three groups; healthy subjects, diabetic subjects and patients with diabetic retinopathy (DR). The permission for carrying out the study was obtained from ethical review committee. Confidentiality of the data was maintained. The data obtained was analyzed and processed using SPSS software. Results: The mean Fasting Blood Glucose (FBG) levels were found to be 5.51 ± 0.34 (mmol/l), 8.11 ± 0.67 (mmol/l) and 8.73 ± 0.90 (mmol/l) in healthy controls, diabetic subjects and patients with DR respectively (p=0.001). The mean serum homocysteine levels were found to be 10.12 + 1.95 (µmol/l), 24.99 ± 4.25 (µmol/l) and 45.78 + 9.66 (µmol/l) in healthy controls, diabetic subjects and patients with DR respectively (p=0.001). Conclusion: Our research can be concluded that serum homocysteine levels have a strong association with the development of diabetic retinopathy. Monitoring the serum levels of this inflammatory biomarker can therefore be helpful in obviating the development of diabetic microangiopathic complications, particularly diabetic retinopathy. Serum homocystein can be used a prognostic tool in the progression of microangiopathic complications of diabetes.
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46

ANTONIO, M. Celia, C. Marta NUNES, Helga REFSUM, and K. Abraham ABRAHAM. "A novel pathway for the conversion of homocysteine to methionine in eukaryotes." Biochemical Journal 328, no. 1 (November 15, 1997): 165–70. http://dx.doi.org/10.1042/bj3280165.

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Activation of amino acid homocysteine was compared with that of methionine in rabbit crude liver extracts and purified multi-enzyme complex of aminoacyl-tRNA synthetases. Activation was studied by measuring the incorporation of radioactive amino acid into unlabelled trichloroacetic-acid insoluble materials in the absence of protein synthesis. Homocysteine synthetase activity was found in the crude extract and in the purified multi-enzyme complex of aminoacyl-tRNA synthetases. On a molar basis, the activation of methionine by the crude extract was five times higher than the activation of homocysteine. There was a partial loss of Hcy-tRNA synthetase activity in the purified multi-enzyme complex. Preliminary reconstitution experiments indicated a requirement for an additional factor for Hcy-tRNA synthetase activity. TLC of the amino acid released from tRNA charged with [14C]homocysteine, revealed radioactivity in homocysteine, methionine and homocysteine thiolactone, indicating a conversion of tRNA-attached homocysteine to methionine. Total tRNA was separated on a benzoylated cellulose column into a fraction enriched in initiator tRNA and a methionine-accepting, but initiator tRNA-deficient, fraction. Homocysteine-accepting activity was present only in the initiator tRNA-enriched fraction. Based on the above data we propose that homocysteine activation in reticulocyte lysates, reported previously, also occurs in liver. Activated homocysteine is attached to initiator tRNA and then converted to methionine by a methylating enzyme. In the absence of methylation, tRNA-attached homocysteine is hydrolysed to produce homocysteine thiolactone.
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47

Cuskelly, Geraldine J., Peter W. Stacpoole, Jerry Williamson, Thomas G. Baumgartner, and Jesse F. Gregory. "Deficiencies of folate and vitamin B6exert distinct effects on homocysteine, serine, and methionine kinetics." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (December 1, 2001): E1182—E1190. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1182.

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Folate and vitamin B6act in generating methyl groups for homocysteine remethylation, but the kinetic effects of folate or vitamin B6deficiency are not known. We used an intravenous primed, constant infusion of stable isotope-labeled serine, methionine, and leucine to investigate one-carbon metabolism in healthy control ( n = 5), folate-deficient ( n = 4), and vitamin B6-deficient ( n = 5) human subjects. The plasma homocysteine concentration in folate-deficient subjects [15.9 ± 2.1 (SD) μmol/l] was approximately two times that of control (7.4 ± 1.7 μmol/l) and vitamin B6-deficient (7.7 ± 2.1 μmol/l) subjects. The rate of methionine synthesis by homocysteine remethylation was depressed ( P = 0.027) in folate deficiency but not in vitamin B6deficiency. For all subjects, the homocysteine remethylation rate was not significantly associated with plasma homocysteine concentration ( r = −0.44, P = 0.12). The fractional synthesis rate of homocysteine from methionine was positively correlated with plasma homocysteine concentration ( r = 0.60, P= 0.031), and a model incorporating both homocysteine remethylation and synthesis rates closely predicted plasma homocysteine levels ( r = 0.85, P = 0.0015). Rates of homocysteine remethylation and serine synthesis were inversely correlated ( r = −0.89, P < 0.001). These studies demonstrate distinctly different metabolic consequences of vitamin B6and folate deficiencies.
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48

Jakubowski, Hieronim. "Facile syntheses of [35S]homocysteine-thiolactone, [35S]homocystine, [35S]homocysteine, and [S-nitroso-35S]homocysteine." Analytical Biochemistry 370, no. 1 (November 2007): 124–26. http://dx.doi.org/10.1016/j.ab.2007.05.030.

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49

STEAD, Lori M., Margaret E. BROSNAN, and John T. BROSNAN. "Characterization of homocysteine metabolism in the rat liver." Biochemical Journal 350, no. 3 (September 8, 2000): 685–92. http://dx.doi.org/10.1042/bj3500685.

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Recent evidence suggests that an increased plasma concentration of the sulphur amino acid homocysteine is a risk factor for the development of vascular disease. The tissue(s) responsible for homocysteine production and export to the plasma are not well known. However, given the central role of the liver in amino acid metabolism, we developed a rat primary hepatocyte model in which homocysteine (and cysteine) production and export were examined. The dependence of homocysteine export from incubated hepatocytes on methionine concentration fitted well to a rectangular hyperbola, with half-maximal homocysteine export achieved at methionine concentrations of approx. 0.44mM. Hepatocytes incubated with 1mM methionine and 1mM serine (a substrate for the transulphuration pathway of homocysteine removal) produced and exported significantly less homocysteine (25–40%) compared with cells incubated with 1mM methionine alone. The effects of dietary protein on homocysteine metabolism were also examined. Rats fed a 60% protein diet had a significantly increased total plasma homocysteine level compared with rats fed a 20% protein diet. Invitro effects of dietary protein were examined using hepatocytes isolated from animals maintained on these diets. When incubated with 1mM methionine, hepatocytes from rats fed the high protein diet exported significantly more homocysteine compared with hepatocytes from rats fed the normal protein diet. Inclusion of serine significantly lowered homocysteine export in the normal protein group, but the effect was more marked in the high protein group. Invivo effects of serine were also examined. Rats fed a high protein diet enriched with serine had significantly lower total plasma homocysteine (25–30%) compared with controls. These data indicate a significant role for the liver in the regulation of plasma homocysteine levels.
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50

Rasyid, Al, Mohammad Kurniawan, Taufik Mesiano, Rakhmad Hidayat, and Salim Harris. "Association of High Blood Homocysteine and Risk of Increased Severity of Ischemic Stroke Events." International Journal of Angiology 28, no. 01 (July 26, 2018): 034–38. http://dx.doi.org/10.1055/s-0038-1667141.

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AbstractStroke is the leading cause of death and disability in the world as well as in Indonesia. Initial stroke severity is an important factor that affects short- and long-term stroke outcomes. This cross-sectional study was conducted in Cipto Mangunkusumo Hospital from July 2017 to January 2018 to investigate the factors that affect stroke severity. A total of 77 acute ischemic stroke patients were divided into three groups, which include low blood homocysteine levels (< 9 μmol/L), moderate blood homocysteine levels (9–15 μmol/L), and high blood homocysteine levels (> 15 μmol/L). The acquired data were analyzed using Kruskal–Wallis test and a significant difference of initial National Institute of Health Stroke Scale (NIHSS) and blood homocysteine levels (H = 13.328, p = 0.001) were seen, with a mean rank of 25.86 for low blood homocysteine levels, 33.69 for moderate blood homocysteine levels, and 48.94 for high blood homocysteine levels. The patients were then divided into two groups based on the NIHSS (≤5 and > 5) to calculate the risk correlation of blood homocysteine levels and NIHSS by using regression. We found that patients with high blood homocysteine levels had 14.4 times higher risk of having NIHSS > 5 compared with those with low blood homocysteine levels (p = 0.002, 95% confidence interval [CI] [2.714–76.407]), and 3.9 times higher risk compared with those with moderate blood homocysteine levels (p = 0.011, 95% CI [1.371–11.246]). We concluded that homocysteine is a risk factor for a higher stroke severity. Future studies to evaluate the usefulness of homocysteine-lowering therapy in stroke patients are recommended.
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