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Journal articles on the topic 'Cytochrome P-450 Genetic aspects'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Setko, N. P., I. I. Berezin, T. V. Gorohova, A. G. Setko, and S. V. Movergoz. "Molecular-genetic and physiological aspects of workers’ adaptation to industrial environment factors." Sanitarnyj vrač (Sanitary Doctor), no. 9 (September 12, 2022): 673–79. http://dx.doi.org/10.33920/med-08-2209-06.

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Molecular genetic studies of cytochrome P-450 genes and assessment of biological adaptation were carried out in 243 machinists and 202 sinkers employed in underground works. It is shown that the processes of adaptation to the factors of the production environment depend on the functionality of regulatory systems and on the characteristics of genetic associations. It was found that 15.3 % of machinists and 15.3 % of sinkers had a satisfactory level of adaptation, tension and an unsatisfactory level — 38.5 % of machinists and 84.6 % of sinkers; only 46.2 % of machinists failed to adapt. At the same time, up to 60 % of drifters had heterozygous mutations of the cytochrome P-450 genes, which provide effective adaptation to changing factors in the production environment, and up to 84.2 % of machinists had homozygous mutations.

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Roumak, V. S., N. V. Umnova, and G. A. Sofronov. "MOLECULAR AND CELLULAR ASPECTS OF DIOXIN TOXICITY." Annals of the Russian academy of medical sciences 69, no. 3-4 (August 21, 2015): 77–84. http://dx.doi.org/10.15690/vramn.v69.i3-4.1000.

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Background: Using methods of molecular toxicology to study dioxin intoxication consequences the contribution was accessed of pathologic alterations induced and manifested by specific biomarkers and ecogenetic effects among Vietnamese population living on contaminated territories. The causes of variability in individual sensitivity to toxic activity were also evaluated. Materials and methods: Individual biomedical indices were compared between those living in contaminated with dioxins (n =8142) and control (n =4421) regions. Dioxin concentrations were measured by high resolution chromato-mass spectrometry (84 samples). The characteristics of cytochrome P-450 system state (94 persons) and cytogenetic parameters (368 persons, 331 450 cells) reflected the molecular and genetic effects. Variable sensitivity to dioxins was demonstrated by associations of genetic polymorphism (CYP1A1, GSTM1, GSTT1, n =195) and congenital morphogenetic variants among children (n =1734). Results: Numerous consequences were demonstrated among the exposed individuals: noticeable absobtion of dioxins from environmental objects; direct effects of P-450 system’s induction; systemic alterations in nucleus and genetic stability; changes in cellular generation’s rate. The associations were revealed of genetic polymorphism in xenobiotic biotransformation / detoxification system and the peculiarities of development and morphogenesis among exposed children. Conclusion: Characteristics of population chronicle intoxication with dioxins permitted to describe its numerous preclinical and clinical manifestations, to show the key elements in pathogenesis of revealed alterations. Future investigations are to create the groundwork for developing a method for prevention of dioxin pathology induction and realization based on revealing preclinical signs and effects of intoxication.

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Sychev, Dmitry A., Igor N. Sychev, Karin B. Mirzaev, Eric I. Rytkin, Dmitriy V. Ivashchenko, Irina V. Bure, and Vitaliy A. Otdelenov. "Clinical pharmacology technologies for personalization of cardiovascular diseases drug treatment: focus on direct oral anticoagulants." Annals of the Russian academy of medical sciences 74, no. 5 (December 4, 2019): 299–306. http://dx.doi.org/10.15690/vramn1214.

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One of the main causes for adverse reactions development is not taking into account the pharmacokinetics of drugs and the dose. Pharmacokinetics of drugs is mostly defined by the cytochrome P-450 isoenzymes activity, carboxylesterases and many other isoenzymes of drug metabolism, as well as ADME transporters (P-gp etc.) which take part in the process of drug metabolism. The activity of these isoenzymes is defined by the genetic aspects of patients and non-genetic aspects such as comorbidity and drug-drug interactions. The development of complex algorithms for personalization of therapy based on the results of pharmacogenetic studies and in the form of a decision support system will play an important role in reduction of adverse drug reactions. A lot can be achieved for personalization of Direct Oral Anticoagulants for treatment of cardiovascular diseases. New approaches are being developed based on the results of pharmacogenetic and pharmacokinetic testing that will help diminish adverse effects of drugs.

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Resál, T., K. Farkas, and T. Molnár. "P546 The safety and efficacy of the new-generation budesonide-MMX in the aspect of the cytochrome P-450 enzyme genotype." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S516. http://dx.doi.org/10.1093/ecco-jcc/jjab076.667.

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Abstract Background Unlike previous forms of budesonide absorbing from the ileal and ascending colon region, the new-generation budesonide-MMX contains a formula, that allows absorption throughout the whole colon. Budesonide is degraded in the liver by cytochrome P450 3A enzyme, but so far, there is no study examining the relationship between the budesonide’s effect and the enzyme activity. CYP3A5 is absent in 90% of the European/caucasian population due to a functional loss mutation (CYP3A5*3), whereas patients with the wild-type CYP3A5*1 allele may be expected to have increased metabolism. The most common genetic polymorphisms in CYP3A4 (CYP3A4*1B and CYP3A4*22) result in increased and decreased expression, respectively. Methods We enrolled 33 patients with UC in this prospective study until January of 2021. Patients received 9 mg oral budesonide-MMX once daily until 8 weeks. Laboratory parameters (cholesterol, triglyceride, CRP) and serum hormone levels (parathormone, dehydroepiandrosterone and cortisol) were monitored before and after the 8-week therapy to follow metabolic and hormonal changes. During these visits, body composition analysis was also performed with InBody 770 machine to observe the adverse effects of budesonide-MMX in respect of body fat mass, body mass index, protein content of the body and bone mineral content. We examined the CYP450 3A (CYP3A5 and CYP3A4) enzyme genotype of the patients, to see, whether the different alleles of this drug-degrading enzyme affect the efficacy and safety. Results 33 patients had received the 2-month therapy. By the end of follow-up, based on partial Mayo score, 26 (78.8%) patients experienced remission and 6 patients (18.2%) were primary non-responders. Mean pMayo score decreased from 4.18 to 1.63 (p<0.001). No significant changes were observable regarding body composition. Serum cholesterol level showed significant increase (p<0.001), while triglyceride and CRP did not show significant changes. Serum cortisol levels were decreased (p<0.001), while PTH and DHEA showed no significant decrease. Only two patients experienced side effects: one of them hypertonia, headache and acnes, while the other mild diarrhoea. 3 patients have CYP3A5*1/*3 genotype, and 16 have CYP3A5*3/*3. There was no significant difference between the two groups, regarding safety and efficacy. Only 1 patient have CYP3A4*1B genotype, while the rest have CYP3A4*1, hence, no statistics could be performed. Conclusion In our study, budesonide-MMX proved to be safe and effective in the therapy of UC, however, cholesterol was elevated in the serum. Based on our cohort, different genotypes of CYP3A don’t have an impact on the effect of the drug, however, CYP3A allele variants are rare, therefore, further examinations should be performed.

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Savelyeva, Marina I., Ekaterina O. Golubenko, Zhannet A. Sozaeva, Irina V. Poddubnaya, and Vera V. Korennaya. "Analysis of the complications of endocrine therapy with tamoxifen in breast cancer: clinical and pharmacogenetic aspects. Prospective pharmacogenetic cohort study." Journal of Modern Oncology 24, no. 3 (November 25, 2022): 361–67. http://dx.doi.org/10.26442/18151434.2022.3.201783.

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Background. Tamoxifen is the drug of choice in ER-positive breast cancer (BC) therapy for perimenopausal women and one of the endocrine therapy options for menopausal patients. The pharmacological effect of tamoxifen can be influenced by the activity of cytochrome P450 (CYP) enzymes and P-glycoprotein transporters (Pg), and the genes encoding them have broad polymorphism, affecting serum concentrations of active metabolites. This article presents the overall results of a prospective population-based study of the clinical significance of genetic polymorphism of tamoxifen metabolic enzymes and transporters in breast cancer patients after radical treatment receiving adjuvant endocrine therapy with tamoxifen in outpatient settings during 2018-2019. The study was approved by the Research Ethics Committee of the Russian Medical Academy of Continuing Professional Education. Aim. To analyze the clinical presentation of endocrine therapy with tamoxifen in the adjuvant regimen and to assess the association of polymorphisms of genes encoding cytochrome P450 enzymes and drug transporter proteins with adverse events in BC patients. Materials and methods. One hundred and four women with stage I-III luminal breast cancer receiving adjuvant tamoxifen were examined for the presence of CYP2D6, CYP2C, and the following CYP3A gene polymorphisms: CYP2D6*4, CYP3A5*3, CYP2C9*2, CYP2C9*3, CYP2C19*2, CYP2C19*3, as well as the ABCB1 gene polymorphic marker (C3435T) encoding the P-glycoprotein. The allelic variants were identified using the real-time polymerase chain reaction; the test was performed in the Research Center of the Russian Medical Academy of Continuing Professional Education. The study material was buccal epithelium (double sampling) taken after informed consent signing. Results. Association analysis showed the association of different genetic polymorphisms of CYP2D6, CYP3A5, CYP2C9, and ABCB1 with tamoxifen adverse drug reactions, indicating the clinical significance of these polymorphisms. Conclusion. With the implementation of genetic testing of the studied polymorphisms into the routine clinical practice of oncologists prescribing tamoxifen and gynecologists involved in the follow-up of breast cancer patients receiving endocrine therapy in the adjuvant mode, there will be an opportunity for more effective and safer pharmacotherapy.

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Mancilla-Morales, Misael D., Santiago Romero-Fernández, Araceli Contreras-Rodríguez, José J. Flores-Martínez, Víctor Sánchez-Cordero, L. Gerardo Herrera M., María F. López, and Enrico A. Ruiz. "Diverging Genetic Structure of Coexisting Populations of the Black Storm-Petrel and the Least Storm-Petrel in the Gulf of California." Tropical Conservation Science 13 (January 2020): 194008292094917. http://dx.doi.org/10.1177/1940082920949177.

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Estimations on the influence of evolutionary and ecological forces as drivers of population gene diversity and genetic structure have been performed on a growing number of colonial seabirds, but many remain poorly studied. In particular, the population genetic structure of storm-petrels (Hydrobatidae) has been evaluated in only a few of the 24 recognized species. We assessed the genetic diversity and population structure of the Black Storm-Petrel ( Hydrobates melania) and the Least Storm-Petrel ( Hydrobates microsoma) in the Gulf of California. The two species were selected because they are pelagic seabirds with comparable ecological traits and breeding grounds. Recent threats such as introduced species of predators and human disturbance have resulted in a decline of many insular vertebrate populations in this region and affected many different aspects of their life histories (ranging from reproductive success to mate selection), with a concomitant loss of genetic diversity. To elucidate to what extent the population genetic structure occurs in H. melania and H. microsoma, we used 719 base pairs from the mitochondrial cytochrome oxidase c subunit I gene. The evaluation of their molecular diversity, genetic structure, and gene flow were performed through diversity indices, analyses of molecular and spatial variance, and isolation by distance (IBD) across sampling sites, respectively. The population genetic structure (via AMOVA and SAMOVA) and isolation by distance (pairwise p-distances and FST/1– FST (using ΦST) were inferred for H. microsoma. However, for H. melania evidence was inconclusive. We discuss explanations leading to divergent population genetic structure signatures in these species, and the consequences for their conservation.

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Setsune, J. I., and D. Dolphin. "Organometallic aspects of cytochrome P-450 metabolism." Canadian Journal of Chemistry 65, no. 3 (March 1, 1987): 459–67. http://dx.doi.org/10.1139/v87-080.

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Carbeneiron porphyrins, (N,Fe)-bridged methyleneiron porphyrins, N-alkyliron porphyrins and σ-alkyliron porphyrins have all been shown to occur in nature and to be interconvertible via redox reactions. The chemistry of the naturally occurring iron porphyrins and model iron, cobalt, and ruthenium porphyrins is reviewed emphasizing their organometallic chemistry.

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Miles, J. S., A. W. Munro, B. N. Rospendowski, W. E. Smith, J. McKnight, and A. J. Thomson. "Domains of the catalytically self-sufficient cytochrome P-450 BM-3. Genetic construction, overexpression, purification and spectroscopic characterization." Biochemical Journal 288, no. 2 (December 1, 1992): 503–9. http://dx.doi.org/10.1042/bj2880503.

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1. The gene CYP102 encoding cytochrome P-450 BM-3 and subgenes encoding the cytochrome P-450 and cytochrome P-450 reductase domains have been cloned in Escherichia coli. 2. The protein products of these genes have been overexpressed and purified to homogeneity. 3. The cytochrome P-450 domain is purified in the ferric low-spin state, but is readily converted into the high-spin state by addition of the substrate palmitate (Ks = 1 microM). The cytochrome P-450 reductase domain readily reduces cytochrome c. Mixing the two domains reconstitutes only about one-thousandth of the fatty acid hydroxylase activity associated with the intact cytochrome P-450 BM-3. 4. The X-band e.p.r. spectra of both the cytochrome P-450 domain and intact cytochrome P-450 BM-3 give g-values indicating low-spin ferric haem. The spectra are virtually identical with those of the equivalent form of cytochrome P-450 cam indicating that the haem ligation in cytochrome P-450 BM-3 is identical with that of cytochrome P-450 cam. 5. Resonance Raman spectra of the substrate-free and substrate-bound forms of the cytochrome P-450 domain are given. Spectral differences in comparison with cytochrome P-450 cam may reflect subtle electronic differences between the respective haem environments.

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Cusato, J., D. G. Ribaldone, L. Bertani, M. Antonucci, C. Tomasello, G. P. Caviglia, S. Dibetto, M. Mangia, M. Astegiano, and A. D’Avolio. "DOP20 Genetic of vitamin D as predictor of response to adalimumab in Crohn’s Disease." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S058—S061. http://dx.doi.org/10.1093/ecco-jcc/jjab073.059.

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Abstract Background Personalised medicine is the direction towards are converging many efforts of experts in inflammatory bowel diseases (IBDs). The advent of biological drugs, with anti-TNF as first category, have revolutionized the managements of these patients. Unfortunately, several unmet needs are present, like an efficacy in about two third of the patients, onset of side effects like infections, paradoxical IMIDs. Being able to treat with these drugs only patients who will respond would avoid losing time without disease improvement and possible side effects. Vitamin D is important for several biological functions, such as regulation of the immune response and modulation of expression of genes encoding enzymes and transporters involved in drug metabolism and transport. Vitamin D is activated by cytochrome (CYP) 27B1, inactivated by CYP24A1, transported in kidney by Vitamin D binding protein (VDBP, encoded by GC gene) and carries out its activities through its receptor (VDR). No data are available concerning vitamin D genetics and response to anti-TNF drug adalimumab. The aim of this study was to describe the relationship between vitamin D pathway-related gene single nucleotide polymorphisms (SNPs) and adalimumab clinical outcome in a cohort of patients affected by Crohn’s disease. Methods We performed a multi-centre prospective study including patients affected by Crohn’s disease who started adalimumab therapy. SNPs in CYP27B1, CYP24A1, GC and VDR genes were analysed. Clinical outcome was considered as clinical response and remission at 3 months of therapy. Results We enrolled 69 patients. Median age was 40 (IQR 31–56) years, males were 40 (58%). Median basal calprotectin was 396 (IQR 188–851) mg/Kg, and 36 (53.7%) had a positive PCR value. We documented the following associations: CYP27B1 + 2838 CT/TT with perianal disease (p= 0.002), basal calprotectin (p= 0.018) and T3 calprotectin (p= 0.035), figure 1; CYP27B1-1260 GT/TT with perianal disease (p= 0.006), basal calprotectin (p= 0.036) and T3 calprotectin (p= 0.024); VDR ApaI CA/AA with basal calprotectin (p= 0.014) and T3 calprotectin (p= 0.036); VDR BsmI GA/AA with perianal disease (p= 0.036), and GC 1296 TG/GG with basal calprotectin (p= 0.014), figure 2. GC 1296 TG/GG genotype polymorphism (p= 0.044, figure 3) predicted clinical remission at multivariate analysis. Finally, median concentrations adalimumab trough levels at 3 months were 7.4 (IQR 5.5; 11.7) ug/mL. CYP24A1 3999 (p=0.025) and VDR TaqI (p=0.016) SNPs affected these levels. Conclusion This is the first study reporting the association between vitamin D pathway-related genetics and adalimumab treatment in a cohort of patients affected by IBD. Further studies in different and larger cohorts are needed to clarify these aspects.

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Abdalwahhab, Omir, Asmaa Galal-Khallaf, Samy Abd El-Latif Saber, Alaa GM Osman, and Khaled Mohammed-Geba. "A case study for application of DNA barcoding in identifying species and genetic diversity of fish from the Suez city market, Egypt." Aquatic Living Resources 33 (2020): 11. http://dx.doi.org/10.1051/alr/2020012.

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The Red Sea is one of the key areas of biodiversity in the world. It is a hotspot for speciation and biological invasions. In the current work, a pilot, random sampling trial was carried out to characterize some species in the landings reaching the fish market in Suez city, which is one of the largest fish markets in the Northern Red Sea. Samples of different fish species were subjected to the standard procedures of DNA barcoding, applying the sequencing of the cytochrome oxidase subunit 1 mitochondrial gene (COI). DNA barcoding could successfully identify all the targeted fishes to the species-level (>98%). The results exhibited a taxonomically-versatile commercial trends in this market, being the collected species belonging to 7 different fish families and 3 orders. These species were Coris aygula, Papilloculiceps longiceps, Priacanthus sagittarious, Gerres longirostris, Alepes djedaba, Psettodes erumei Cheilinus trilobatus, Calotomus viridescens, and Pardachirus marmoratus. Haplotype diversities in the first six species were moderate. However, their nucleotide diversities were low. This may have resulted from fishing from bottlenecked populations, or from areas that do not hinder the genetic flow. Also, possible cryptic speciation could be detected in P. sagittarius, P. erumei and G. longirostris. Applying the DNA barcoding for species identification in Suez city fish market could then detect various aspects of fish species diversity. More works using the applied analyses can be strongly recommended to aid proper conservation and management of economic fisheries in the Red Sea.

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Mansour, H., M. Levacher, E. Azoulay-Dupuis, J. Moreau, C. Marquetty, and M. A. Gougerot-Pocidalo. "Genetic differences in response to pulmonary cytochrome P-450 inducers and oxygen toxicity." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1376–81. http://dx.doi.org/10.1152/jappl.1988.64.4.1376.

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The effects of cytochrome P-450 inducers on O2 toxicity were studied in mice. We first examined three cytochrome P-450 inducers, which differ by their specific tissue affinity: phenobarbital sodium (PB), essentially active in the liver, and 3-methylcholanthrene (3-MC) and beta-naphthoflavone (BNF), which are also active in the lung. Both BNF and 3-MC increased the survival rate and significantly decreased pulmonary edema (pulmonary water and wet-to-dry weight ratio) in C57BL/6J mice exposed to hyperoxia (O2 greater than or equal to 95%), whereas PB had no protective effect. In the second part of this study, we compared the action of BNF in two strains of mice. In one (C57BL/6J), cytochrome P-450 can be induced by aromatic hydrocarbons, whereas in the other (DBA/2J) cytochrome P-450 is not inducible by these compounds. Protection against O2 toxicity was assessed in terms of lethality and pulmonary edema and of lung lipid peroxidation (assessed by measuring malondialdehyde). BNF only protected against O2 toxicity in the inducible strain. This protective effect of BNF on O2 toxicity in C57BL/6J mice was associated mainly with a large increase in the components of the cytochrome P-450 system (cytochrome P-450 and cytochrome b5) in the lung. The activity of pulmonary superoxide dismutase was also slightly increased, but the enhancement was not statistically significant. In contrast, in DBA/2J mice neither the components of the cytochrome P-450 system nor the activity of superoxide dismutase showed any increase.(ABSTRACT TRUNCATED AT 250 WORDS)

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DAMON, Marie, Alain FAUTREL, André GUILLOUZO, and Laurent CORCOS. "Genetic analysis of the phenobarbital regulation of the cytochrome P-450 2b-9 and aldehyde dehydrogenase type 2 mRNAs in mouse liver." Biochemical Journal 317, no. 2 (July 15, 1996): 481–86. http://dx.doi.org/10.1042/bj3170481.

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The aim of this study was to investigate the effect of the genetic background on the phenobarbital inducibility of cytochrome P-450 2b-9, cytochrome P-450 2b-10 and aldehyde dehydrogenase type 2 mRNAs in mice. We analysed the basal expression and the phenobarbital inducibility of both cytochrome P-450 mRNAs by semi-quantitative specific reverse transcription-PCR analyses in five inbred mouse strains (A/J, BALB/cByJ, C57BL/6J, DBA/2J and SWR/J). Male mice constitutively expressed cytochrome P-450 2b-9 and cytochrome P-450 2b-10 mRNAs, but a number of differences in their response to phenobarbital were observed. In all these mouse strains, phenobarbital induced cytochrome P-450 2b-10 mRNA whereas it could have either a positive or a negative effect on cytochrome P-450 2b-9 expression, depending on the strain and the sex of the mice. Specifically, phenobarbital increased cytochrome P-450 2b-9 expression in C57BL/6J males while it decreased it in DBA/2J mice. Interestingly, dexamethasone was able to mimic the phenobarbital effect on both cytochromes P-450 in these two strains. Aldehyde dehydrogenase type 2 mRNA was always induced by phenobarbital, except in the C57BL/6J strain. Genetic analysis revealed that the phenobarbital-inducible phenotype was either a semi-dominant or a recessive trait in F1 animals from a C57BL/6J×DBA/2J cross for the cytochrome P-450 2b-9 and the aldehyde dehydrogenase type 2 genes, respectively. This study suggests that the genetic basis for phenobarbital induction in mice depends on the target gene, and that more than one regulatory step would be involved in this response pathway.

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BEREWELA, DIA AHAK M. "The Pharmacogenetics of Cytochrome P-450 and its Effect on Drug Metabolism." Journal of Drug Delivery and Therapeutics 10, no. 5-s (October 15, 2020): 219–23. http://dx.doi.org/10.22270/jddt.v10i5-s.4473.

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Cytochrome P-450 (CYP-450) enzyme plays an essential role in the oxidation of most drugs, and thus it can affect the toxicity and efficacy of many medications. Factors that influence the function and presence of cytochrome have a key impact on the outcomes of therapy. More specifically, characteristics of cytochrome pharmacogenetics and procedures of cytochrome enzymes induction and inhibition can greatly influence the rate of drug biotransformation and the rate of elimination. So, an understanding of genetic variants which are associated with drug responses and illnesses could improve and enhance the outcome of treatment. Clinical data in genetic tests may be useful in order to develop methods for assessing genetic risks. Positively, genetic tests for monogenic sicknesses have already proven to be a useful test and any changes may trigger a new field of personalized drug. This review will look at the influence of pharmacogenetics in drug metabolism and the importance of using personal genetic data in achieving optimal therapy and in preventing any possible adverse effects. Keywords: Pharmacogenetics, Biotransformation, CYP-450

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Hernando-Rodriguez, Miriam, Natalia Rey-Barja, Xabier Marichalar-Mendia, Maria J. Rodriguez-Tojo, Amelia Acha-Sagredo, and Jose M. Aguirre-Urizar. "Role of cytochrome P-450 genetic polymorphisms in oral carcinogenesis." Journal of Oral Pathology & Medicine 41, no. 1 (July 28, 2011): 1–8. http://dx.doi.org/10.1111/j.1600-0714.2011.01067.x.

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Kalow, W. "Genetic variation in the human hepatic cytochrome P-450 system." European Journal of Clinical Pharmacology 31, no. 6 (1987): 633–41. http://dx.doi.org/10.1007/bf00541288.

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Kapitulnik, J., J. P. Hardwick, J. D. Ostrow, C. C. Webster, S. S. Park, and H. V. Gelboin. "Increase in a specific cytochrome P-450 isoenzyme in the liver of congenitally jaundiced Gunn rats." Biochemical Journal 242, no. 1 (February 15, 1987): 297–300. http://dx.doi.org/10.1042/bj2420297.

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Congenitally jaundiced (jj) Gunn rats had a greater hepatic microsomal content of a cytochrome P-450 isoenzyme, P-450c, than did the non-jaundiced (Jj) rats. No differences in content of P-450b, P-450d and pregnenolone-16 alpha-carbonitrile-induced (PCN) P-450 were found between jj and Jj rats. This is the first demonstration of a constitutive increase in a specific cytochrome P-450 isoenzyme in association with a genetic defect.

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Hällström, Inger, and Agneta Blanck. "Genetic regulation of the cytochrome P-450 system in Drosophila melanogaster. I. Chromosomal determination of some cytochrome P-450-dependent reactions." Chemico-Biological Interactions 56, no. 2-3 (December 1985): 157–71. http://dx.doi.org/10.1016/0009-2797(85)90003-1.

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Hällström, I. "Genetic regulation of the cytochrome P-450 system in Drosophila melanogaster. II. Localization of some genes regulating cytochrome P-450 activity." Chemico-Biological Interactions 56, no. 2-3 (December 1985): 173–84. http://dx.doi.org/10.1016/0009-2797(85)90004-3.

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Daraki, Aggeliki, Sophia Zachaki, Theodora Koromila, Maria Karakosta, Gabriel Pantelias, Vasiliki Aleporou, Constantina Sambani, Panagoula Kollia, and Kalliopi Manola. "the G516 Polymorphism of Cytochrome P450 2B6 Gene in the Susceptibility of De Novo Acute Myeloid Leukemia." Blood 120, no. 21 (November 16, 2012): 2513. http://dx.doi.org/10.1182/blood.v120.21.2513.2513.

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Abstract Abstract 2513 Acute myeloid leukemia (AML) is a heterogeneous disease with well-known clinical and pathological aspects, characterized by the acquisition of somatic mutations in haematopoietic progenitors leading to disruption of differentiation. However, the genetic etiology of AML, which include gene mutations and chromosomal aberrations, is largely unknown. Altered forms of genes that differ by a single nucleotide polymorphisms (SNPs) have been shown to predispose individuals to AML development. Recently it has been reported that interindividual differences based on detoxification genes polymorphisms may contribute to the AML susceptibility. Human cytochrome P450 (CYP) enzymes play a key role as phase I enzymes in the metabolism of drugs and environmental chemicals. Several CYP enzymes metabolically activate procarcinogens to genotoxic intermediates. CYP2B6 blocks the transformation of precarcinogens to their biologically active forms that provoke chromosomal instability and leukemia. CYP2B6 G516T SNP change the aminoacid sequence (Gln172His), resulting in enzymatic inactivation. Thus, individuals homozygous for the mutant allele (T/T) or heterozygotes (G/T) present decreased enzymatic activity. We performed a case-control study in a large series of AML patients to investigate the potential relation between genotype of CYP2B6 G516T SNP and the risk of de novo AML. We also compared the genotypic frequencies in AML patients in respect to chromosome abnormalities, FAB classification and clinical characteristics. The CYP2B6 G516T genotyping was performed on 195 de novo AML patients at diagnosis and 215 sex and age matched healthy controls using a PCR-RFLP assay and LightSNP assay. Unstimulated bone marrow cells were used for karyotypic analysis and karyotypes were described according to ISCN. Statistical analysis was performed using Chi-square test and P<0.05 was considered to be statistically significant. Karyotypic analysis was successfully performed in 97.8% of AML patients at diagnosis. Among them, 136 (69.7%) showed clonal karyotypic abnormalities. The genotypic distribution in patients and healthy groups was statistically significant and showed: homozygous wild type G/G 54,5% vs 67.2%, heterozygotes G/T 40.4% vs 27.5% and homozygous mutant T/T 6.7% vs 5.5% respectively (p<0.05). Stratification of patients according to FAB classification revealed differences in CYP2B6 genotype (p=0.069), which focuses primarily on an increase frequency of heterozygotes G/T in AML-M2 patients (61.4% vs 27.5%, p=0.000) and homozygous mutant T/T in AML-M6 patients (40% vs 5.4%, p=0.006).No differences in genotypic distribution of CYP2B6 genotype was noticed between male and female AML patients or among AML patients and healthy control group. Among females, the frequency of the mutant variant T was significantly increased in AML patients comparing to the healthy subjects (p=0.024).Interestingly, patients with aberrations of chromosomes 5 and/or 7 [−5/del(5q), −7/del(7q)], which confer a poor prognosis, showed a statistically increased frequency of the homozygous mutant T/T genotype in contrast to patients with favorable prognosis chromosome abnormalities such as inv(16), t(8;21), t(15;17) (p=0.044). The increased frequency of mutant allele leading to reduced enzyme activity suggests that the CYP2B6 gene may be a predisposing factor for the development of AML. Furthermore, the CYP2B6 G516T polymorphism seems to be associated with the presence of lesions on chromosomes 5 and / or 7 which are poor prognostic lesions in AML. Therefore, the high frequency of mutant genotypes (G/T and T/T) of CYP2B6 G516T SNP in these cytogenetic groups may be involved in the development of these specific chromosomal abnormalities. Disclosures: No relevant conflicts of interest to declare.

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Hällström, Inger. "Genetic variation in cytochrome P-450-dependent demethylation in Drosophila melanogaster." Biochemical Pharmacology 36, no. 14 (July 1987): 2279–82. http://dx.doi.org/10.1016/0006-2952(87)90591-0.

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21

Gates, Brian J., and Neal M. Davies. "AmpliChip for Cytochrome P-450 Genotyping: The Epoch of Personalized Prescriptions." Hospital Pharmacy 41, no. 5 (May 2006): 442–54. http://dx.doi.org/10.1310/hpj4105-442.

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The clinical importance of genetic polymorphisms in drug metabolism is well-known in clinical pharmacotherapy. The first widely available pharmacogenomic microarray technology approved by the Food and Drug Administration as a medical device to clinically genotype genetic polymorphisms in drug metabolism is now available with the launch of AmpliChip technology. This readily accessible clinical microarray test allows the genotyping of cytochrome (CYP) P-450 2D6 and 2C19 and marks a milestone in the epoch of evidence based personalized medicine. Many commonly used drugs are substrates for CYP2D6 and CYP 2C19 and hence may potentially demonstrate phenotypic differences as poor, intermediate, extensive, and ultrarapid metabolizers. These phenotypic variations could lead to expressed differences in pharmacotherapeutic patient outcomes. AmpliChip currently allows for testing of multiple alleles (31) in a single assay. Other technologies for pharmacogenomics are on the horizon. This article reviews the importance of polymorphic enzymes and genotyping as to how genetic polymorphisms alter pharmacotherapy and the emergence of a plethora of technologies that may become routinely available for clinical pharmacogenomic testing in the near future.

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22

Gonder, J. C., R. A. Proctor, and J. A. Will. "Genetic differences in oxygen toxicity are correlated with cytochrome P-450 inducibility." Proceedings of the National Academy of Sciences 82, no. 18 (September 1, 1985): 6315–19. http://dx.doi.org/10.1073/pnas.82.18.6315.

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23

Meier, U. Thomas, and Urs A. Meyer. "Genetic polymorphism of human cytochrome P-450 (S)-mephenytoin 4-hydroxylase. Studies with human autoantibodies suggest a functionally altered cytochrome P-450 isozyme as cause of the genetic deficiency." Biochemistry 26, no. 25 (December 1987): 8466–74. http://dx.doi.org/10.1021/bi00399a065.

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24

GUENGERICH, F. PETER, PHILIPPE H. BEAUNE, DIANE R. UMBENHAUER, PERRY F. CHURCHILL, RICHARD W. BORK, GHAZI A. DANNAN, ROBERT G. KNODELL, R. STEPHEN LLOYD, and MARTHA V. MARTIN. "Cytochrome P-450 enzymes involved in genetic polymorphism of drug oxidation in humans." Biochemical Society Transactions 15, no. 4 (August 1, 1987): 576–78. http://dx.doi.org/10.1042/bst0150576.

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SALLEE, FLOYD R., C. LINDSAY DeVANE, and ROBERT E. FERRELL. "Fluoxetine-Related Death in a Child with Cytochrome P-450 2D6 Genetic Deficiency." Journal of Child and Adolescent Psychopharmacology 10, no. 1 (January 2000): 27–34. http://dx.doi.org/10.1089/cap.2000.10.27.

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26

Bilal, Rabiea, Naseem Saud, and Sualeha Riffat. "Rasagiline Pharmacokinetics are affected by cytochrome P-450 1A2 genetic variants in different doses." Proceedings for Annual Meeting of The Japanese Pharmacological Society 93 (2020): 2—O—039. http://dx.doi.org/10.1254/jpssuppl.93.0_2-o-039.

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27

Choi, Jun, Byung-Gun Kim, Ai-Young Lee, Min-Jung Kim, and Won-Young Chey. "Genetic polymorphism of cytochrome P 450 2C9 in diphenylhydantoin-induced cutaneous adverse drug reactions." European Journal of Clinical Pharmacology 60, no. 3 (May 1, 2004): 155–59. http://dx.doi.org/10.1007/s00228-004-0753-0.

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28

Li, Dailin, Roger Belusa, Susana Nowicki, and Anita Aperia. "Arachidonic acid metabolic pathways regulating activity of renal Na+-K+-ATPase are age dependent." American Journal of Physiology-Renal Physiology 278, no. 5 (May 1, 2000): F823—F829. http://dx.doi.org/10.1152/ajprenal.2000.278.5.f823.

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Locally formed arachidonic acid (AA) metabolites are important as modulators of many aspects of renal tubular function, including regulation of the activity of tubular Na+-K+-ATPase. Here we examined the ontogeny of the AA metabolic pathways regulating proximal convoluted tubular (PCT) Na+-K+-ATPase activity in infant and adult rats. Eicosatetraynoic acid, an inhibitor of all AA-metabolizing pathways, abolished this effect. AA inhibition of PCT Na+-K+-ATPase was blocked by the 12-lipoxygenase inhibitor baicalein in infant but not in adult rats and by the specific cytochrome P-450 fatty acid ω-hydroxylase inhibitor 17-octadecynoic acid in adult but not in infant rats. The lipoxygenase metabolite 12(S)-hydroxyeicosatetraenoic acid (HETE) and the cytochrome P-450 metabolite 20-HETE both inhibited PCT Na+-K+-ATPase in a protein kinase C-dependent manner, but the effect was significantly more pronounced in infant PCT. Lipoxygenase mRNA was only detected in infant cortex. Expression of renal isoforms of cytochrome P-450 mRNA was more prominent in adult cortex. In summary, the AA metabolic pathways that modulated the activity of rat renal proximal tubular Na+-K+-ATPase are age dependent.

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Sokolov, D. A., Pavel A. Lyuboshevskiy, N. Yu Levshin, A. V. Zhemchugov, and L. V. Kuptsova. "The influence of cytochrome p-450 gene polymorphisms on the tramadol postoperative analgesia effectiveness." Regional Anesthesia and Acute Pain Management 10, no. 3 (September 15, 2016): 192–96. http://dx.doi.org/10.18821/1993-6508-2016-10-3-192-196.

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The effectiveness of postoperative analgesia may be determined by genetic characteristics of patients that affect the pharmacodynamics and pharmacokinetics of drugs. In particular, as a result of the metabolism of tramadol by isoenzyme of cytochrome P-450 is formed O-desmethyltramadol having higher affinity to mu-opioid receptors. The paper explored the effectiveness of analgesia based on tramadol in 48 patients after endoscopic gynecological surgery depending on the presence/absence of polymorphisms of CYP2D6 gene.It was found that 15 patients with polymorphisms С100Т and G1846A had more intensive postoperative pain, which was accompanied by activation of the sympathetic nervous system. Determination of these polymorphisms may be useful to select the optimal postoperative analgesia.

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Vorobyeva, N. A., and A. I. Vorobyeva. "CYTOCHROME P-450 AND VKORC1 GENETIC POLYMORPHISMS IN NENETS - AN INDIGENOUS ETHNIC GROUP IN THE ARCTIC." Human Ecology, no. 9 (September 18, 2020): 11–17. http://dx.doi.org/10.33396/1728-0869-2020-9-11-17.

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31

Mihajlović, Filip, Aleksandar Milosavljević, and Jagoda Gavrilović. "The impact of genetic polymorphism of cytochrome p-450 2C9 and 1A2 isoforms on warfarine metabolism." Medicinski casopis 52, no. 2 (2018): 68–78. http://dx.doi.org/10.5937/mckg52-17406.

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32

Lee, M. S. "Role of genetic polymorphisms related to neurotransmitters and cytochrome P-450 enzymes in response to antidepressants." Drugs of Today 43, no. 8 (2007): 569. http://dx.doi.org/10.1358/dot.2007.43.8.1130447.

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33

Shibata, N., T. Ohnuma, H. Baba, H. Shimada, T. Takahashi, and H. Arai. "Genetic association between cytochrome P-450 2D6 gene polymorphism and plasma concentration of haloperidolin Japanese schizophrenics." Psychiatric Genetics 9, no. 3 (September 1999): 145–48. http://dx.doi.org/10.1097/00041444-199909000-00006.

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34

Katoch, Meenu, M. A. Hussain, and A. Ahuja. "Comparison of SSR and cytochrome P-450 markers for estimating genetic diversity in Picrorhiza kurrooa L." Plant Systematics and Evolution 299, no. 9 (May 5, 2013): 1637–43. http://dx.doi.org/10.1007/s00606-013-0820-z.

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35

von Borstel, R. C., D. F. O'Connell, R. D. Mehta, and U. G. G. Hennig. "Modulation in cytochrome P-420 and P-450 content in Saccharomyces cerevisiae according to physiological conditions and genetic background." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 150, no. 1-2 (June 1985): 217–24. http://dx.doi.org/10.1016/0027-5107(85)90118-6.

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36

Santos, Jaqueline Rocha Borges dos, Larrysa de Morais Alves da Cruz, Luís Phillipe Nagem Lopes, and Maria Eline Matheus. "Tobacco consumption during the COVID-19 pandemic and pharmacokinetic interaction involving cytochrome P-450 with psychoactive drugs: an integrative review." Research, Society and Development 11, no. 10 (July 28, 2022): e222111032349. http://dx.doi.org/10.33448/rsd-v11i10.32349.

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This integrative review examines tobacco use related to mental disorders in COVID-19 pandemic and potential interactions involving cytochrome P-450 between tobacco and psychotropic drugs. The five steps of the integrative review development process were considered, namely: elaboration of the guiding question, literature search or sampling, evaluation of data, data analysis, interpretation and presentation of results. A literature search was performed in the Medline and Bireme databases, without language restrictions up to May 2021. Forty-seven articles were found with information on COVID-19, tobacco use and psychiatric illness. Articles were also sought that addressed interactions between major classes of psychotropic drugs and tobacco associated with CYP450 isoforms and genetic polymorphism. Thirty-seven articles were found for interaction among tobacco, cytochrome P450 and antidepressants; 7 including polymorphism; 19 articles involving interaction of tobacco, cytochrome P450 and antipsychotics; 4 including polymorphism; 3 articles describing interaction of tobacco, cytochrome P450 and anxiolytics; 1 including polymorphism; 2 articles regarding interaction of tobacco, cytochrome P450 and mood stabilizers; and 1 including polymorphism. These findings reinforce the importance of recognizing the role of tobacco associated with drug use in mental disorders; indicating the need for monitoring to prevent worsening clinical conditions.

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37

Selvin, Steve. "Cytochrome P450 1A1 Polymorphism and Childhood Leukemia: An Analysis of Matched Pairs Case-Control Genotype Data." Cancer Epidemiology, Biomarkers & Prevention 13, no. 8 (August 1, 2004): 1371–74. http://dx.doi.org/10.1158/1055-9965.1371.13.8.

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Abstract The association between the genotypic frequencies of the cytochrome P450 1A1 polymorphism and the risk of childhood leukemia is explored with the data from a matched case-control study. The data are displayed in a 3 × 3 case-control array, and the discordant pair counts are assessed for quasi-independence, homogeneity, and symmetry. This statistical approach is contrasted to the more typical analysis of matched data based on a conditional logistic model and estimated odds ratios. The statistical analysis of 175 matched pairs (part of a large study of potential environmental/genetic influences on the risk of childhood leukemia) showed no evidence of an association between cytochrome P450 1A1 genotype frequencies and case-control status.

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38

Chhun, Stéphanie, Céline Verstuyft, Nathalie Rizzo-Padoin, Guy Simoneau, Laurent Becquemont, Jean François Bergmann, and Stéphane Mouly. "The Cytochrome P-450 2C9/2C19 but Not the ABCB1 Genetic Polymorphism May Be Associated With the Liver Cytochrome 3A4 Induction by Phenytoin." Journal of Clinical Psychopharmacology 32, no. 3 (June 2012): 429–31. http://dx.doi.org/10.1097/jcp.0b013e3182549c0c.

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39

Stapleton, Phoebe A., Adam G. Goodwill, Milinda E. James, and Jefferson C. Frisbee. "Altered mechanisms of endothelium-dependent dilation in skeletal muscle arterioles with genetic hypercholesterolemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (September 2007): R1110—R1119. http://dx.doi.org/10.1152/ajpregu.00410.2007.

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With most cardiovascular disease risk factors, endothelium-dependent dilation of skeletal muscle resistance arterioles is compromised, although with hypercholesterolemia, impairments to reactivity are not consistently observed. Using apolipoprotein E (ApoE) and low-density lipoprotein receptor (LDLR) gene deletion male mouse models of hypercholesterolemia at 20 wk of age, we tested the hypothesis that arteriolar dilation would be maintained due to an increased stimulus-induced production of dilator metabolites via cyclooxygenase and cytochrome P-450 epoxygenase pathways. Arterioles from both strains demonstrated mild reductions in dilation to hypoxia and acetylcholine versus responses in C57/Bl/6J (C57) controls. However, although inhibition of nitric oxide synthase (NOS) attenuated dilation in arterioles from C57 controls, this effect was absent in ApoE or LDLR strains. In contrast, cyclooxygenase-dependent portions of dilator reactivity were maintained across the three strains. Notably, although combined NOS and cyclooxygenase inhibition abolished arteriolar responses to hypoxia and acetylcholine in C57 controls, significant reactivity remained in ApoE and LDLR strains. Whereas inhibition of cytochrome P-450 ω-hydroxylase and epoxygenases had no effect on this residual reactivity in ApoE and LDLR strains, inhibition of 12/15-lipoxygenase with nordihydroguaiaretic acid abolished the residual reactivity. With both hypoxic and methacholine challenges, arteries from ApoE and LDLR strains demonstrated an increased production of both 12( S)- and 15( S)-hydroxyeicosatetraenoic acid, end products of arachidonic acid metabolism via 12/15-lipoxygenase, a response that was not present in C57 controls. These results suggest that with development of hypercholesterolemia, mechanisms contributing to dilator reactivity in skeletal muscle arterioles are modified such that net reactivity to endothelium-dependent stimuli is largely intact.

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40

Haslemo, T., and L. Tanum. "Use of antidepressants in a modern globalized society." Die Psychiatrie 7, no. 03 (July 2010): 162–68. http://dx.doi.org/10.1055/s-0038-1669572.

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SummaryDepression is a highly prevalent condition throughout the world. Ethnicity is reported to influence treatment outcome with antidepressants in a number of ways, including both cultural and genetic factors. Non-genetic factors such as the type of diet, beliefs about depression and attitudes towards treatment with antidepressants are proposed to directly influence medication adherence and the rate of remission. Genetic factors are mainly expressed through inter-individual variance in drug metabolism and must be born in mind when antidepressants are prescribed in a multi-ethnic society. Recent advances in molecular biology have revealed substantial variance in the Cytochrome-P450 enzyme system, which is considered to be the most important and relevant factor for ethnic variance in the metabolism. This underscores the usefulness of therapeutic drug monitoring and individualization of treatment in clinical practice. This paper will briefly review factors related to ethnicity that may be of potential importance for treatment outcome and with a special emphasis on the ethnical diversity of cytochrome P-450 enzyme systems.

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Sokolov, D. A., Pavel A. Lyuboshevskiy, and A. N. Ganert. "INFLUENCE OF CYTOCHROME P-450 GENETIC POLYMORPHISMS ON THE MAIN AND SIDE EFFECTS OF TRAMADOL IN THE POSTOPERATIVE PERIOD." Regional Anesthesia and Acute Pain Management 11, no. 4 (December 15, 2017): 240–46. http://dx.doi.org/10.18821/1993-6508-2017-11-4-240-246.

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One of the approaches to increasing the effectiveness and safety of postoperative analgesia can be its personification. The goal of the study was to evaluate the efficacy of tramadol analgesia depending on the polymorphisms of the CYP2D6 gene, the cytochrome P-450 isoenzyme, involved in drug biotransformation into the active metabolite. 96 patients with elective endoscopic gynecology procedures were examined. Polymorphisms G1846A and C100T, which reduce the activity of the isoenzyme CYP2D6, were detected, and the intensity of postoperative pain, the autonomic nervous system state by cardiointervalography and hemostasis using rotational thromboelastometry were evaluated. Polymorphisms were detected in 29 (30.2%) patients, united in the 1-st group. The second group consisted of 67 patients without gene polymorphisms. Patients with polymorphisms have a higher pain scores; the frequency of postoperative nausea and vomiting, on the contrary, was significantly lower. According to cardiointervalography, sympathicotonia was observed in Group 1 patients after surgery, while in Group 2 patients the indices did not change significantly compared to baseline. The parameters of hemostasis in patients of the 2nd group were characterized by moderate hypercoagulability (shortening of clotting time and clot formation time), whereas in the firsts group, relative hypocoagulation (decrease in α angle, and clot firmness) was noted. Conclusion. In female carriers of G1846A and C100T polymorphisms of the CYP2D6 gene, the effectiveness of post-operative analgesia based on tramadol is reduced. They have a lower incidence of postoperative nausea and vomiting, and moderate hypocoagulation. Probably, these phenomena are associated with a change in the ratio between the drug and its active metabolite - O-desmethyltramadol.

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42

Yenny, Yenny. "Pharmacokinetic interactions between rifampicin and efavirenz in HIV-TB coinfections." Universa Medicina 28, no. 3 (February 29, 2016): 188–201. http://dx.doi.org/10.18051/univmed.2009.v28.188-201.

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The increased percentage of patients with HIV-TB coinfection leads to inevitable interactions between rifampicin and efavirenz. Efavirenz is a potent non-nucleoside reverse transcriptase inhibitor (NNRTI) for the treatment of HIV infection. The use of this drug combination with rifampicin causes problems in determination of the optimal dosage of efavirenz when administered concomitantly with rifampicin. Efavirenz is metabolized by the enzyme cytochrome P-450 (CYP), i.e. the CYP2B6 and CYP3A4 isozymes, of which rifampicin is an inducer. The induction of cytochrome P-450 by rifampicin is mediated by pregnane X (PXR) and constitutive androstane receptors (CAR) in the cell nucleus, resulting in a wide variation in the plasma efavirenz concentrations, such that a therapeutic failure or the occurrence of toxic effects are to be expected. The optimal dosage of efavirenz is commonly determined through pharmacokinetic studies, but this is problematic in the combined use of the drug with rifampicin, due to the wide variation in study design, method, and sample size of each study. Ethnic factors and genetic polymorphism of the enzymes that metabolize efavirenz contribute to the problem of determining the optimal dose of this drug. Pharmacokinetic studies with good measurement parameters and methods are still necessary as the basis for determining the optimal dose of efavirenz in the Indonesian population.

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43

Zohir, Naguib, Reham Afifi, Asmaa Ahmed, Zinab Aly, Mehry Elsobekey, Heba Kareem, and Rehab Helmy. "Role of CYP2C9, VKORC1 and Calumenin Genotypes in Monitoring Warfarin Therapy: An Egyptian Study." Open Access Macedonian Journal of Medical Sciences 1, no. 1 (December 15, 2013): 76–82. http://dx.doi.org/10.3889/oamjms.2013.015.

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Background: Oral anticoagulant therapy is conditioned by environmental and genetic factors.Objectives: To verify the effect of the calumenin, cytochrome P-450 variants and VKORC1 genetic polymorphisms on the response to warfarin therapy and warfarin dose adjustment.Patients and Methods: We selected fifty warfarin treated patients with dose adjusted at INR value between 2 and 3. PCR-RFLP is used for of calumenin gene polymorphism. Insitu Hybridization was used for identification of VKORC1 promoter and CYP2C9 variants polymorphisms.Results: The warfarin dose in the patients with Calumenin and CYP2C9 genetic polymorphism was lower than the wild type gene. The warfarin dose in the patients with VKORC1 variants was statistically lower compared to that of the wild-type. The presence of combined CYP2C9 genetic variants and VKORC1 polymorphism was associated with lower warfarin dose than that the wild types.Conclusion: Calumenin (CALU) might be a new genetic factor involved in the pharmacogenetics of anticoagulant therapy.

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44

Mohammed, HossamY K., YousryZ Al-Zohairy, and Mahmoud AbdEl-Latif Hashish. "The effect of ‘cytochrome P-450 2C9’ and ‘vitamin K epoxide reductase complex 1’ genetic polymorphism upon oral anticoagulation requirements." Al-Azhar Assiut Medical Journal 16, no. 4 (2018): 371. http://dx.doi.org/10.4103/azmj.azmj_91_18.

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45

Chan, Andrew T., Gregory J. Tranah, Edward L. Giovannucci, David J. Hunter, and Charles S. Fuchs. "A prospective study of genetic polymorphisms in the cytochrome P-450 2C9 enzyme and the risk for distal colorectal adenoma." Clinical Gastroenterology and Hepatology 2, no. 8 (August 2004): 704–12. http://dx.doi.org/10.1016/s1542-3565(04)00294-0.

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46

Deloria, Laurel, Viola Abbott, Nigel Gooderham, and Gilbert J. Mannering. "Induction of xanthine oxidase and depression of cytochrome P-450 by interferon inducers: Genetic difference in the responses of mice." Biochemical and Biophysical Research Communications 131, no. 1 (August 1985): 109–14. http://dx.doi.org/10.1016/0006-291x(85)91777-2.

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47

Hlavica, Peter, and Michael Lehnerer. "Some aspects of the role of cytochrome P-450 isozymes in the n-oxidative transformation of secondary and tertiary amine compounds." Journal of Biochemical Toxicology 10, no. 5 (October 1995): 275–85. http://dx.doi.org/10.1002/jbt.2570100508.

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48

Kahn, GC, AR Boobis, MJ Brodie, EL Toverud, S. Murray, and DS Davies. "Phenacetin O-deethylase: an activity of a cytochrome P-450 showing genetic linkage with that catalysing the 4-hydroxylation of debrisoquine?" British Journal of Clinical Pharmacology 20, no. 1 (July 1985): 67–76. http://dx.doi.org/10.1111/j.1365-2125.1985.tb02800.x.

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49

Roman, Richard J. "P-450 Metabolites of Arachidonic Acid in the Control of Cardiovascular Function." Physiological Reviews 82, no. 1 (January 1, 2002): 131–85. http://dx.doi.org/10.1152/physrev.00021.2001.

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Recent studies have indicated that arachidonic acid is primarily metabolized by cytochrome P-450 (CYP) enzymes in the brain, lung, kidney, and peripheral vasculature to 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) and that these compounds play critical roles in the regulation of renal, pulmonary, and cardiac function and vascular tone. EETs are endothelium-derived vasodilators that hyperpolarize vascular smooth muscle (VSM) cells by activating K+channels. 20-HETE is a vasoconstrictor produced in VSM cells that reduces the open-state probability of Ca2+-activated K+channels. Inhibitors of the formation of 20-HETE block the myogenic response of renal, cerebral, and skeletal muscle arterioles in vitro and autoregulation of renal and cerebral blood flow in vivo. They also block tubuloglomerular feedback responses in vivo and the vasoconstrictor response to elevations in tissue Po2both in vivo and in vitro. The formation of 20-HETE in VSM is stimulated by angiotensin II and endothelin and is inhibited by nitric oxide (NO) and carbon monoxide (CO). Blockade of the formation of 20-HETE attenuates the vascular responses to angiotensin II, endothelin, norepinephrine, NO, and CO. In the kidney, EETs and 20-HETE are produced in the proximal tubule and the thick ascending loop of Henle. They regulate Na+transport in these nephron segments. 20-HETE also contributes to the mitogenic effects of a variety of growth factors in VSM, renal epithelial, and mesangial cells. The production of EETs and 20-HETE is altered in experimental and genetic models of hypertension, diabetes, uremia, toxemia of pregnancy, and hepatorenal syndrome. Given the importance of this pathway in the control of cardiovascular function, it is likely that CYP metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with some of these conditions and that drugs that modify the formation and/or actions of EETs and 20-HETE may have therapeutic benefits.

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50

Setko, N. P., A. G. Setko, Ekaterina V. Bulycheva, A. V. Tyurin, and E. Yu Kalinina. "Polymorphism of p-450 cytochrome detoxication genes in adolescents depending on the degree of contamination of the organism by heavy metals." Hygiene and sanitation 99, no. 5 (July 7, 2020): 478–82. http://dx.doi.org/10.47470/0016-9900-2020-99-5-478-482.

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Introduction. Changes in the body of children and adolescents aimed at adapting to environmental factors are determined by genetic polymorphism in xenobiotic biotransformation genes, determining the degree of susceptibility of the child’s body to pollutants, which is the basis of modern personalized preventive medicine when managing risks to the health of the child population under the influence of environmental factors. Material and methods. Trace elements, including heavy metals, lead and cadmium, were determined in the hair of 256 practically healthy teenagers by atomic absorption spectrophotometry. Depending on the level of content of the latter, two groups of adolescents were formed to determine six genes of the cytochrome P-450 family. Group 1 consisted of adolescents whose cadmium lead content exceeded the average Russian indices. The second group included adolescents whose heavy metals were above the level of average Russian standards. Results. Studies have shown that in adolescents of the 1st group, compared with the data of adolescents of the 2nd group, an increase in the number of carriers of two mutant alleles at the locus rs 1048943 (gene CYP1A1) is 3.08 times, rs 464621 (gene CYP1A1) is 1. 8 times; locus rs 2069522 (CYP1A2 gene) 3.63 times; locus rs 1799853 (CYP2C9 * 2 gene) 4.5 times; locus rs 1057910 (gene CYP2C9 * 3) 3.8 times and locus rs 2279343 (gene CYP2B6) 4.25 times. Moreover, carriers of two normal alleles in adolescents of the first group at the locus rs 1048943 (gene CYP1A1) were 5.14 times; locus rs 2279343 (CYP2B6 gene) was 6.5 fold less than among adolescents of the 2nd group; and at the locus rs 464621 (gene CYP1A1), rs 2069522 (gene CYP1A2), rs 1799853 (gene CYP2C9 * 2), rs 1057910 (gene CYP2C9 * 3) there were no carriers of normal homozygotes. Conclusion. Group 1 adolescents with heavy metal contamination of the body are carriers significantly in a greater number of pathological mutations in the genes of the cytochrome P-450 detoxification system in comparison with data from group 2 adolescents.

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