Drug Metabolizing Enzymes As a Causal Factor in the Inter-species Differences in Drug Action.

1995 ◽  
Vol 10 (3) ◽  
pp. 372-385
Author(s):  
TETSUYA KAMATAKI
Keyword(s):  
Species Differences ◽  
Drug Action ◽  
Causal Factor ◽  
Drug Metabolizing Enzymes ◽  
Metabolizing Enzymes

Species Differences in the Response of Liver Drug-Metabolizing Enzymes to (S)-4-O-Tolylsulfanyl-2-(4-trifluormethyl-phenoxy)-butyric Acid (EMD 392949) in Vivo and in Vitro

2008 ◽  
Vol 36 (4) ◽  
pp. 702-714 ◽  
Author(s):  
Lysiane Richert ◽  
Gregor Tuschl ◽  
Catherine Viollon-Abadie ◽  
Nadège Blanchard ◽  
Alexandre Bonet ◽  
...  
Keyword(s):  
Butyric Acid ◽  
Species Differences ◽  
Drug Metabolizing Enzymes ◽  
Metabolizing Enzymes

scholarly journals Pharmacogenomics in depression and antidepressants

2005 ◽  
Vol 7 (3) ◽  
pp. 223-230
Keyword(s):  
Side Effects ◽  
Adverse Effects ◽  
Drug Response ◽  
Genetic Factors ◽  
Drug Action ◽  
Mechanisms Of Action ◽  
Drug Metabolizing Enzymes ◽  
Receptor Function ◽  
Metabolizing Enzymes ◽  
Adaptive Processes

Genetic factors are believed to play a major role in the variation of treatment response and the incidence of adverse effects to medication. The aim of pharmacogenetics is to elucidate this variability according to hereditary differences. Considering current hypotheses for the mechanisms of action of antidepressants, most investigations to date have concentrated on mutations in genes coding either for the pathways in the serotonergic and noradrenergic systems or for drug-metabolizing enzymes. Recent studies shifted the emphasis on the main mechanism of drug action from changes in neurotransmitter concentration or receptor function toward long-lasting adaptive processes within the neurons. Although the results are controversial, many studies support the hypothesis that psychopharmacogenetics will help predict an individual's drug response, while minimizing the side effects. The inclusion of functional genomics, which investigates the complex gene and/or protein expression in response to a given drug, may lead to the development of novel and safer drugs.

scholarly journals Species Differences in the Distribution of Drug-Metabolizing Enzymes in the Pancreas

2002 ◽  
Vol 30 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Alexis B. Ulrich ◽  
Jens Standop ◽  
Bruno M. Schmied ◽  
Matthias B. Schneider ◽  
Terence A. Lawson ◽  
...  
Keyword(s):  
Species Differences ◽  
Drug Metabolizing Enzymes ◽  
Metabolizing Enzymes

Analysis of the Potential Association of Drug-Metabolizing Enzymes CYP2C9*3 and CYP2C19*3 Gene Variations With Type 2 Diabetes: A Case-Control Study

2020 ◽  
Vol 21 (14) ◽  
pp. 1152-1160
Author(s):  
Imadeldin Elfaki ◽  
Rashid Mir ◽  
Faisel Mohammed Abu-Duhier ◽  
Chandan Kumar Jha ◽  
Adel Ibrahim Ahmad Al-Alawy ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Antiplatelet Drug ◽  
Drug Metabolizing Enzymes ◽  
Genotype Distribution ◽  
Nucleotide Polymorphisms ◽  
Metabolizing Enzymes ◽  
Specific Pcr ◽  
Increased Risk ◽  
Different Populations

Background:: Cytochrome P450s (CYPs) are drug-metabolizing enzymes catalyzing the metabolism of about 75% of drug in clinical use. CYP2C9 represents 20% CYP proteins in liver cells and is a crucial member of CYPs superfamily. CYP2C19 metabolizes very important drugs such as antiulcer drug omeprazole, the antiplatelet drug clopidogrel and anticonvulsant mephenytoin. Single nucleotide polymorphisms (SNPs) of CYP genes have been associated with unexpected drug reactions and diseases in different populations. Objective:: We examined the associations of CYP2C9*3 (rs1057910) and CYP2C19*3 (rs4986893) with T2D in Saudi population. Methods:: We used the allele-specific PCR (AS-PCR) and DNA sequencing in 111 cases and 104 controls for rs1057910, and in 119 cases and 110 controls for rs4986893. Results:: It is indicated that the genotype distribution of rs1057910 in cases and controls were not significantly different (P=0.0001). The genotypes of rs1057910 were not associated with type 2 diabetes (T2D) (P>0.05). Whereas the genotype distribution of rs4986893 in cases and controls was significantly different (P=0.049). The AA genotype of rs4986893 may be associated in increased risk to T2D with OR=17.25 (2.06-143.8), RR=6.14(0.96-39.20), P=0.008. Conclusion:: The CYP2C9*3 (rs1057910) may not be associated with T2D, while CYP2C19*3 (rs4986893) is probably associated with T2D. These findings need to be validated in follow-up studies with larger sample sizes and different populations.

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