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Journal articles on the topic 'Methotrexate Toxicology'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Slørdal, L., R. Jaeger, J. Kjaeve, and J. Aarbakke. "Pharmacokinetics of 7-Hydroxy-methotrexate and Methotrexate in the Rat." Pharmacology & Toxicology 63, no. 2 (August 1988): 81–84. http://dx.doi.org/10.1111/j.1600-0773.1988.tb00915.x.

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2

UNDP/UNFPA/WHO/World Bank Special P. "Methotrexate for the termination of early pregnancy: a toxicology review." Reproductive Health Matters 5, no. 9 (January 1997): 162–67. http://dx.doi.org/10.1016/s0968-8080(97)90020-3.

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3

Armagan, A., E. Uzar, E. Uz, HR Yilmaz, S. Kutluhan, HR Koyuncuoglu, S. Soyupek, H. Cam, and TA Serel. "Caffeic acid phenethyl ester modulates methotrexate-induced oxidative stress in testes of rat." Human & Experimental Toxicology 27, no. 7 (July 2008): 547–52. http://dx.doi.org/10.1177/0960327108092293.

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The aim of this study was to investigate the possible protective role of caffeic acid phenethyl ester on testicular toxicity of methotrexate in rats. Nineteen male rats were divided into three groups as follows: group I, control; group II, methotrexate-treated; group III, methotrexate + caffeic acid phenethyl ester-treated. In the second day of experiment, a single dose of methotrexate was intraperitoneally administered to groups II and III, although a daily single dose of caffeic acid phenethyl ester was intraperitoneally administered to group III for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. In the tissue, the level of lipid peroxidation as malondialdehyde and activities of superoxide dismutase were higher in the methotrexate group than in the control group. Lipid peroxidation levels and superoxide dismutase activities were decreased in caffeic acid phenethyl ester + methotrexate group compared with methotrexate group. The activities of catalase in the methotrexate group decreased insignificantly although its activities were significantly increased by caffeic acid phenethyl ester administration. The activity of glutathione peroxidase did not change in the groups. There was significant difference in body weight between control and methotrexate-induced groups. In conclusion, the administration of methotrexate causes elevation of oxidative stress although treatment with caffeic acid phenethyl ester has protective effects on the oxidative stress in testes.

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4

Bardin, Philip G., David J. Fraenkel, and Richard W. Beasley. "Methotrexate in Asthma." Drug Safety 9, no. 3 (September 1993): 151–55. http://dx.doi.org/10.2165/00002018-199309030-00002.

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5

Gökçe, Ahmet, Suleyman Oktar, Ahmet Koc, and Zafer Yonden. "Protective effects of thymoquinone against methotrexate-induced testicular injury." Human & Experimental Toxicology 30, no. 8 (September 2, 2010): 897–903. http://dx.doi.org/10.1177/0960327110382564.

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Thymoquinone is the major active component derived from Nigella sativa. Methotrexate is a folic acid antagonist widely used in clinic. Aim of this study was to investigate the possible protective role of thymoquinone on testicular toxicity of methotrexate. Experiments were performed on male C57BL/6 mice (6 weeks old, 20 ± 2 g). The animals were divided into four groups with six mice in each group. Equivalent volumes of saline were injected intraperitoneally (i.p.) in the control group. In the thymoquinone group, mice received thymoquinone i.p. with a dose of 10 mg/kg/day for 4 days. Mice in the methotrexate group received single dose of methotrexate i.p., with a dose of 20 mg/kg. Finally, in the methotrexate plus thymoquinone group, in the first and the following 3 days after methotrexate administration, thymoquinone was injected with a dose of 10 mg/kg/day, i.p. At the end of the experiment, the left testis was quickly removed and divided into two parts for histological examination and biochemical analysis. Methotrexate alone increased total antioxidant capacity and myeloperoxidase activity compared to the controls. Thymoquinone treatment decreased total antioxidant capacity and prevented the increase in the myeloperoxidase activity. Light microscopy showed in mice that receiving methotrexate resulted in interstitial space dilatation, edema, severe disruption of the seminiferous epithelium and reduced diameter of the seminiferous tubules. Administration of thymoquinone reversed histological changes of methotrexate significantly. We suggest that thymoquinone use may decrease the destructive effects of methotrexate on testicular tissue of patients using this agent.

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6

Roy(Pal), Madhumita, Sharmila Sengupta, Rita Ghosh, Nitao P. Bhattacharyya, Subrata K. Dey, and Sukhendu B. Bhattacharjee. "Characterisation of methotrexate-resistant clones." Mutation Research/Environmental Mutagenesis and Related Subjects 291, no. 1 (February 1993): 43–51. http://dx.doi.org/10.1016/0165-1161(93)90016-s.

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7

Angelova, E., M. Krsnik-Rasol, M. Biruš, and D. Papeš. "Methotrexate effects on plant cells." Mutation Research/Environmental Mutagenesis and Related Subjects 271, no. 2 (1992): 148. http://dx.doi.org/10.1016/0165-1161(92)91162-k.

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8

Raveendran, R., W. Heybroek, M. Caulfield, M. Lawson, S. M. L. Abrams, P. F. M. Wrigley, M. Slevin, and P. Turner. "Indomethacin and Protein Binding of Methotrexate." Human & Experimental Toxicology 11, no. 4 (July 1992): 291–93. http://dx.doi.org/10.1177/096032719201100411.

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Indomethacin, a non-steroidal anti-inflammatory drug is known to increase the efficacy and toxicity of methotrexate, the widely used anti-cancer drug in man. The mechanism for this interaction has not been clearly established. However, since these drugs bind with albumin, a possible displacement of methotrexate by indomethacin from albumin might explain this interaction. To investigate the possible interaction an in-vitro protein-binding displacement study was carried out in 17 normal volunteers and in two groups of eight cancer patients. One group of patients had active disease and the other was in complete clinical remission. Serum samples were obtained and protein levels estimated. The protein binding of methotrexate was measured alone and with indomethacin using equilibrium dialysis. Statistical analysis of results suggested that the binding of methotrexate is not influenced by indomethacin, confirming that methotrexate is not displaced by indomethacin.

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9

LoVecchio, Frank, Kenneth D. Katz, David J. Watts, and Ian O. Wood. "Four-year experience with methotrexate exposures." Journal of Medical Toxicology 4, no. 3 (September 2008): 149–50. http://dx.doi.org/10.1007/bf03161192.

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10

Stockley, Ivan H. "Methotrexate—NSAID interactions." Drug Intelligence & Clinical Pharmacy 21, no. 6 (June 1987): 546. http://dx.doi.org/10.1177/106002808702100617.

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11

Drafi, Frantisek, Katarina Bauerova, Viera Kuncirova, Silvester Ponist, Danica Mihalova, Tatiana Fedorova, Juraj Harmatha, and Radomir Nosal. "Pharmacological influence on processes of adjuvant arthritis: effect of the combination of an antioxidant active substance with methotrexate." Interdisciplinary Toxicology 5, no. 2 (November 9, 2012): 84–91. http://dx.doi.org/10.2478/v10102-012-0015-4.

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Abstract Oxygen metabolism has an important role in the pathogenesis of rheumatoid arthritis. A certain correlation was observed between oxidative stress, arthritis and the immune system. Reactive oxygen species produced in the course of cellular oxidative phosphorylation and by activated phagocytic cells during oxidative burst, exceed the physiological buffering capacity and result in oxidative stress. The excessive production of ROS can damage protein, lipids, nucleic acids, and matrix components. Patients with rheumatoid arthritis have an altered antioxidant defense capacity barrier. In the present study the effect of substances with antioxidative properties, i.e. pinosylvin and carnosine, was determined in monotherapy for the treatment of adjuvant arthritis (AA). Moreover carnosine was evaluated in combination therapy with methotrexate. Rats with AA were administered first pinosylvin (30 mg/kg body mass daily per os), second carnosine (150 mg/kg body mass daily per os) in monotherapy for a period of 28 days. Further, rats with AA were administered methotrexate (0.3 mg/kg body mass 2-times weekly per os), and a combination of methotrexate+carnosine, with the carnosine dose being the same as in the previous experiment. Parameters, i.e. changes in hind paw volume and arthritic score were determined in rats as indicators of destructive arthritis-associated clinical changes. Plasmatic levels of TBARS and lag time of Fe2+- induced lipid peroxidation (tau-FeLP) in plasma and brain were specified as markers of oxidation. Plasmatic level of CRP and activity of γ-glutamyltransferase (GGT) in spleen and joint were used as inflammation markers. In comparison to pinosylvin, administration of carnosine monotherapy led to a significant decrease in the majority of the parameters studied. In the combination treatment with methotrexate+carnosine most parameters monitored were improved more remarkably than by methotrexate alone. Carnosine can increase the disease-modifying effect of methotrexate treatment in rat AA.

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12

Giannini, Edward H., and James T. Cassidy. "Methotrexate in Juvenile Rheumatoid Arthritis." Drug Safety 9, no. 5 (November 1993): 325–39. http://dx.doi.org/10.2165/00002018-199309050-00002.

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13

Bebarta, Vikhyat S., Matthew D. Hensley, and Douglas J. Borys. "Acute Methotrexate Ingestions in Adults: A Report of Serious Clinical Effects and Treatments." Journal of Toxicology 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/214574.

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Objective.Limited reported data have reports effects after acute ingestion of methotrexate. Treatment recommendations do not differentiate between exposure routes. Our objective was to determine the frequency of significant toxicity effects and use of therapy after methotrexate ingestion in adults.Methods.We performed a retrospective study on adult cases reported to 6 poison centers over 6 years (2000–2005) which exceed 180,000 exposures/year. Variables collected included demographics, dosages ingested, coingestions, clinical effects, and therapies with outcomes.Results.Sixty-three patients examined over the 6-year period met inclusion criteria. No patient in the series received dialysis or died. The mean dose ingested for all patients was 24 mg (range 2.5–100 mg) and the mean dose for suicidal ingestions was 47.5 mg (12.5–100 mg). The most common clinical effects were abdominal pain, oral irritation, throat irritation, nausea, dizziness, and headache. Nine patients received folinic acid and 3 patients received sodium bicarbonate. No patient developed renal failure, bone marrow suppression, seizure, or coma. No patient died or received dialysis.Conclusion.In our series of patients from 6 poison centers over six years, 63 cases of acute adult methotrexate ingestions were reported. Methotrexate toxicity from ingestion in adults was uncommon and rarely toxic.

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14

CURD, CHERYL D., JOSEPH E. MANNO, and JOHN J. STEWART. "Effects of Methotrexate on Intestinal Transit in Rats." Toxicological Sciences 5, no. 5 (1985): 991–96. http://dx.doi.org/10.1093/toxsci/5.5.991.

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15

Wolfgang, William J. "Exploring Protection from Methotrexate-Induced Teratogenicity in Flies." Toxicological Sciences 99, no. 2 (October 2007): 363–65. http://dx.doi.org/10.1093/toxsci/kfm198.

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16

CURD, C. "Effects of methotrexate on intestinal transit in rats." Fundamental and Applied Toxicology 5, no. 5 (October 1985): 991–96. http://dx.doi.org/10.1016/0272-0590(85)90181-2.

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17

Remington, Helen St C., and Clifford C. Bailey. "Methotrexate Blood Level Monitoring." Drug Intelligence & Clinical Pharmacy 19, no. 5 (May 1985): 372–73. http://dx.doi.org/10.1177/106002808501900508.

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Methotrexate toxicity can be avoided following high-dose therapy if certain management procedures are adhered to. These include careful fluid balance management and therapeutic drug level monitoring. A case is reported of an episode of methotrexate toxicity resulting from a fluid balance problem.

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18

Severin, María J., Mara S. Trebucobich, Patricia Buszniez, Anabel Brandoni, and Adriana M. Torres. "The urinary excretion of an organic anion transporter as an early biomarker of methotrexate-induced kidney injury." Toxicology Research 5, no. 2 (2016): 530–38. http://dx.doi.org/10.1039/c5tx00436e.

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19

Hendel, J., H. Poulsen, B. Nyfors, and A. Nyfors. "Changes in Liver Histology during Methotrexate Therapy of Psoriasis Correlated to the Concentration of Methotrexate and Folate in Erythrocytes." Acta Pharmacologica et Toxicologica 56, no. 4 (March 13, 2009): 321–26. http://dx.doi.org/10.1111/j.1600-0773.1985.tb01297.x.

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20

Verberne, Eline A., Emma de Haan, J. Peter van Tintelen, Dick Lindhout, and Mieke M. van Haelst. "Fetal methotrexate syndrome: A systematic review of case reports." Reproductive Toxicology 87 (August 2019): 125–39. http://dx.doi.org/10.1016/j.reprotox.2019.05.066.

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21

Affleck, Joslynn G., and Virginia K. Walker. "Transgenic Rescue of Methotrexate-Induced Teratogenicity in Drosophila melanogaster." Toxicological Sciences 99, no. 2 (May 22, 2007): 522–31. http://dx.doi.org/10.1093/toxsci/kfm123.

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22

Chaudhary, Sushma, Manjul Pratap Singh, Chandana Venkateaswara Rao, and Ajay Kumar Singh Rawat. "A Novel Natural Polymers Based Nanoparticles Gel Formulation for the Treatment of Rheumatoid Arthritis: Optimization and In-vivo Evaluation." Drug Delivery Letters 11, no. 2 (June 28, 2021): 164–78. http://dx.doi.org/10.2174/2210303111666210219152401.

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Background: In 1988, the US Food and Drug Administration permitted low dose methotrexate for the treatment of rheumatoid arthritis that would change the progression of the disease. Methotrexate is a folic acid antagonist and its systemic use causes numerous side effects; including hepatic toxicity. It would be preferable to deliver methotrexate by the topical route to reduce side-effects along with ease of administration and reduced dosing frequency. So, nanoparticle gel is a hopeful approach to treat rheumatoid arthritis. Objective: The study aims to develop a nanoparticles gel containing novel natural polymer-based methotrexate nanoparticles and evaluate its therapeutic potential on Complete Freund’s Adjuvant– Induced Arthritis rat model and compare it to methotrexate and dexamethasone gel. Materials and Methods: The five batches of methotrexate nanoparticles gel were prepared viz. F1W2, F2W2, F3W2, F4W2 and methotrexate gel for the topical application by using different concentrations of Carbopol 934 base and characterized for their evaluation parameters: homogeneity, grittiness, pH, spread-ability, viscosity determination, and drug content studies. The arthritic potential of methotrexate-nanoparticles gel was evaluated by Complete Freund’s Adjuvant–Induced Arthritis rats model based on percent inhibition oedema and arthritic score. Result and Discussion: Methotrexate nanoparticles gel significantly reduced the percentage inhibition of oedema compared to methotrexate and dexamethasone gel. The therapeutic activity of nanoparticles gel was found to be F3W2 ≥ F2W2 ≥ F1W2 ≥ F4W2 ≥ MTX gel. So, the optimized nanoparticle gel formulation F3W2 can be effective in the treatment of rheumatoid arthritis. Conclusion: The developed novel nanoparticles gel formulation can be a promising alternative to existing methotrexate and dexamethasone gel.

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23

Del Campo, Miguel, Kenjiro Kosaki, F. C. Bennett, and Kenneth L. Jones. "Developmental delay in fetal aminopterin/methotrexate syndrome." Teratology 60, no. 1 (July 1999): 10–12. http://dx.doi.org/10.1002/(sici)1096-9926(199907)60:1<10::aid-tera5>3.0.co;2-h.

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24

Donnenfeld, Alan E., Anne Pastuszak, Jane Salkoff Noah, Betsy Schick, Nancy C. Rose, and Gideon Koren. "Methotrexate exposure prior to and during pregnancy." Teratology 49, no. 2 (February 1994): 79–81. http://dx.doi.org/10.1002/tera.1420490202.

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25

Schuurman, Henk-Jan, Harold T. Smith, and Emanuele Cozzi. "Tolerability of cyclosphosphamide and methotrexate induction immunosuppression in nonhuman primates." Toxicology 213, no. 1-2 (September 2005): 1–12. http://dx.doi.org/10.1016/j.tox.2005.03.017.

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26

Ezhilarasan, Devaraj. "Hepatotoxic potentials of methotrexate: Understanding the possible toxicological molecular mechanisms." Toxicology 458 (June 2021): 152840. http://dx.doi.org/10.1016/j.tox.2021.152840.

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27

Vericat, J. E. Megías, S. Valero García, M. Amat Díaz, E. López Briz, M. N. Vila Clérigues, and J. L. Poveda Andrés. "Stability of two methotrexate oral formulations." European Journal of Hospital Pharmacy 19, no. 2 (March 12, 2012): 150.1–150. http://dx.doi.org/10.1136/ejhpharm-2012-000074.173.

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28

Benitez, B., E. Capilla, L. Gonzalez, M. P. Garcia de Miguel, C. Rueda, G. Casado, H. Varela, T. Roldan, M. Bravo, and A. Herrero. "Carboxypeptidase rescue after high-dose methotrexate." European Journal of Hospital Pharmacy 19, no. 2 (March 12, 2012): 157.1–157. http://dx.doi.org/10.1136/ejhpharm-2012-000074.189.

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29

Bowen, Donnell, Terry J. Robbins, and Robert M. White. "Interaction of 5?-deoxy-5-fluorouridine and methotrexate." Archives of Toxicology 63, no. 5 (September 1989): 401–5. http://dx.doi.org/10.1007/bf00303130.

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30

González‐Barón, M., M. P. Iniesta, M. I. Sanchez Reus, and B. Ribas. "Anticarcinogenic methotrexate induces metallothionein synthesis†." Toxicological & Environmental Chemistry 13, no. 3-4 (January 1987): 161–70. http://dx.doi.org/10.1080/02772248709357179.

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31

Scanlon, Kevin J., Mohammed Kashani-Sabet, Arlene R. Cashmore, Michele Pallai, Barbara A. Moroson, and Maria Saketos. "The role of methionine in methotrexate-sensitive and methotrexate-resistant mouse leukemia L1210 cells." Cancer Chemotherapy and Pharmacology 19, no. 1 (February 1987): 25–29. http://dx.doi.org/10.1007/bf00296250.

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32

Bremnes, R. M., E. Smeland, N. E. Huseby, T. J. Eide, and J. Aarbakke. "Acute Hepatotoxicity after High-Dose Methotrexate Administration to Rats." Pharmacology & Toxicology 69, no. 2 (August 1991): 132–39. http://dx.doi.org/10.1111/j.1600-0773.1991.tb01286.x.

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33

Finkelstein, Y. "Emergency Treatment of Life-Threatening Intrathecal Methotrexate Overdose." NeuroToxicology 25, no. 3 (March 2004): 407–10. http://dx.doi.org/10.1016/j.neuro.2003.10.004.

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34

Wheeler, Marsha, Patrick O'Meara, and Michelle Stanford. "Fetal methotrexate and misoprostol exposure: The past revisited." Teratology 66, no. 2 (July 22, 2002): 73–76. http://dx.doi.org/10.1002/tera.10052.

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35

Bawle, E. V., J. V. Conard, and L. Weiss. "Adult and two children with fetal methotrexate syndrome." Teratology 57, no. 2 (February 1998): 51–55. http://dx.doi.org/10.1002/(sici)1096-9926(199802)57:2<51::aid-tera2>3.0.co;2-9.

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36

Finkelstein, Yoram, Shoshana Zevin, Bianca Raikhlin-Eisenkraft, and Yedidia Bentur. "Intrathecal methotrexate neurotoxicity: clinical correlates and antidotal treatment." Environmental Toxicology and Pharmacology 19, no. 3 (May 2005): 721–25. http://dx.doi.org/10.1016/j.etap.2004.12.031.

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37

Yawata, Ayako, Saki Kimura, Misato Matsushita, Takehiro Mochizuki, Toshiyuki Chikuma, Hiroshi Hojo, and Yasumitsu Ogra. "Cell-specific Synergic Effect of Cimicifugoside on Cytotoxicity of Methotrexate." JOURNAL OF HEALTH SCIENCE 57, no. 4 (2011): 350–55. http://dx.doi.org/10.1248/jhs.57.350.

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38

Martín, María Cecilia, Pablo Barbero, Boris Groisman, Miguel Ángel Aguirre, and Gideon Koren. "Methotrexate embryopathy after exposure to low weekly doses in early pregnancy." Reproductive Toxicology 43 (January 2014): 26–29. http://dx.doi.org/10.1016/j.reprotox.2013.10.005.

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39

Fuksa, Leos, Eva Brcakova, Gabriela Kolouchova, Petra Hirsova, Milos Hroch, Jolana Cermanova, Frantisek Staud, and Stanislav Micuda. "Dexamethasone reduces methotrexate biliary elimination and potentiates its hepatotoxicity in rats." Toxicology 267, no. 1-3 (January 2010): 165–71. http://dx.doi.org/10.1016/j.tox.2009.11.010.

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40

Wang, Xiuwei, Jianhua Wang, Tao Guan, Qian Xiang, Mingsheng Wang, Zhen Guan, Guannan Li, et al. "Role of methotrexate exposure in apoptosis and proliferation during early neurulation." Journal of Applied Toxicology 34, no. 8 (July 9, 2013): 862–69. http://dx.doi.org/10.1002/jat.2901.

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41

Zhang, Chun-yu, Yuan-xi Feng, Yang Yu, Wen-jing Sun, Jing Bai, Feng Chen, and Song-bin Fu. "The Molecular Mechanism of Resistance to Methotrexate in Mouse Methotrexate-Resistant Cells by Cancer Drug Resistance and Metabolism SuperArray." Basic Clinical Pharmacology Toxicology 99, no. 2 (August 2006): 141–45. http://dx.doi.org/10.1111/j.1742-7843.2006.pto_470.x.

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42

Yuksel, Yasemin, Ramazan Yuksel, Murat Yagmurca, Hacer Haltas, Husamettin Erdamar, Muhsin Toktas, and Osman Ozcan. "Effects of quercetin on methotrexate-induced nephrotoxicity in rats." Human & Experimental Toxicology 36, no. 1 (July 11, 2016): 51–61. http://dx.doi.org/10.1177/0960327116637414.

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Objective: This experimental study was conducted to elucidate the possible protective/therapeutic effects of quercetin against methotrexate (Mtx)-induced kidney toxicity with biochemical and histopathological studies. Methods: Twenty-four adult male rats were randomly divided into four groups, as follows: control group (saline intraperitoneally (i.p.), 9 days), Mtx group (20 mg/kg i.p., single dose), Mtx + quercetin group (50 mg/kg quercetin was orally administered 2 days before and 6 days after Mtx administration) and only quercetin group (50 mg/kg oral, 9 days). Structural changes were evaluated by hematoxylin–eosin and periodic acid–Schiff stainings. Apoptotic changes were investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay and caspase-3 antibody. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured in tissue and plasma samples. Results: Mtx compared with the control group, there was significant increase in nephrotoxic tissue damage findings, in addition to apoptotic index (APOI) and caspase-3 expression ( p < 0.05). Mtx + quercetin group revealed significantly lower histopathological damage and APOI and caspase-3 expression decreased when compared to Mtx group. MDA levels were increased in Mtx group compared to others, and by the use of quercetin, this increase was significantly reduced. SOD levels were higher in Mtx group than others. This increase was evaluated as a relative increase arising from oxidative damage caused by Mtx. Conclusion: As a result, Mtx administration may involve oxidative stress by causing structural and functional damage in kidney tissue in rats. Quercetin reduced the Mtx-induced oxidative stress through its antioxidant properties and so quercetin may be promising to alleviate Mtx-induced renal toxicity.

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43

Nolte, H., and P. Stahl Skov. "Inhibition of basophil histamine release by methotrexate." Agents and Actions 23, no. 3-4 (May 1988): 173–76. http://dx.doi.org/10.1007/bf02142532.

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44

Venkatesan Kotteeswaran, Vidhyutha Srivathsan, Mahima Bhandari, Juanit Thomas E, and Trishita Bhattacharya. "Characterization of Methotrexate Loaded Fucoidan/Chitosan Nanoparticles." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 2644–54. http://dx.doi.org/10.26452/ijrps.v11ispl4.4534.

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Methotrexate is one of the most popular and safe anti-inflammatory drugs which is an antifolate-type antimetabolite and is used as an anticancer drug. In this study, oppositely charged chitosan and fucoidan have been non-covalently bonded using their electrostatic interactions with the methotrexate drug loaded into these nanoparticles. Fucoidan is obtained from marine algae which are composed of l-fucose and sulfate groups in various types of brown seaweeds; whereas chitosan is a naturally occurring biopolymer obtained through the N-deacetylation of chitin. Depending on the fucoidan / chitosan (F / C) weight ratio, three distinct nanoparticles (1F / 1C; 3F / 1C; 5F / 1C) are synthesized and characterized. Nanoparticles were prepared using cross linkers EDC and NHS at a constant pH to reduce the conjugate size. The prepared conjugates were characterized for their size and zeta potential using DLS analysis and the functional groups were analysed using FTIR. DLS results proclaimed that there was size reduction in particle size with cross linker and without the drug methotrexate. The 5:1 F/C nanoparticles was seen to be 441.5 nm, the difference being considerable larger in the 5:1 formulation. Hence for further analysis 5:1 F/C nanoparticles were preferred. Maximum entrapment efficiency was observed in 5:1 F/C nanoparticle with and without cross linkers. To understand the structural morphology of nanoparticles electromagnetic magnification like SEM and TEM were taken in account.

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45

Weitman, Steven D., Gregory J. Kato, Jerry L. Barbosa, and Barton A. Kamen. "Low-dose methotrexate therapy for hepatoblastoma." Cancer Chemotherapy and Pharmacology 28, no. 3 (1991): 233–34. http://dx.doi.org/10.1007/bf00685519.

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Çetiner, Mustafa, Göksel Şener, A. Özer Şehirli, Emel Ekşioğlu-Demiralp, Feriha Ercan, Serap Şirvancı, Nursal Gedik, Sertaç Akpulat, Tülay Tecimer, and Berrak Ç. Yeğen. "Taurine protects against methotrexate-induced toxicity and inhibits leukocyte death." Toxicology and Applied Pharmacology 209, no. 1 (November 2005): 39–50. http://dx.doi.org/10.1016/j.taap.2005.03.009.

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Ibsen, Hans Henning W. "Electroencephalographic Examination in Seven Patients Treated with Methotrexate for Psoriasis." Acta Pharmacologica et Toxicologica 58, no. 4 (March 13, 2009): 303–4. http://dx.doi.org/10.1111/j.1600-0773.1986.tb00113.x.

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Mouridsen, H. T., E. Jacobsen, and O. Faber. "The Pharmacokinetics of Cyclophosphamide in Man Following Treatment with Methotrexate." Acta Pharmacologica et Toxicologica 38, no. 5 (March 13, 2009): 508–12. http://dx.doi.org/10.1111/j.1600-0773.1976.tb03146.x.

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David, N. Bailey, Joseph J. Coffee, and R. Briggs John. "Percutaneous absorption of methotrexate as its sodium salt in vivo." Journal of Toxicology: Cutaneous and Ocular Toxicology 6, no. 1 (January 1987): 9–12. http://dx.doi.org/10.3109/15569528709052159.

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Koçak, Aslıhan Yonca, Oğuzhan Koçak, Figen Aslan, and Mustafa Tektaş. "Methotrexate toxicity presenting as cutaneous ulcerations on psoriatic plaques." Cutaneous and Ocular Toxicology 32, no. 4 (March 28, 2013): 333–35. http://dx.doi.org/10.3109/15569527.2013.779278.

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