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PubMed2003

Genetic polymorphism and trade-offs in the early life-history strategy of the Pacific oyster, Crassostrea gigas (Thunberg, 1795): a quantitative genetic study.

We investigated genetic variability and genetic correlations in early life-history traits of Crassostrea gigas. Larval survival, larval development rate, size at settlement and metamorphosis success were found to be substantially heritable, whereas larval growth rate and juvenile traits were not. We identified a strong positive genetic correlation between larval development rate and size at settlement, and argue that selection could optimize both age and size at settlement. However, trade-offs, resulting in costs of metamorphosing early and large, were suggested by negative genetic correlations or covariances between larval development rate/size at settlement and both metamorphosis success and juvenile survival. Moreover, size advantage at settlement disappeared with time during the juvenile stage. Finally, we observed no genetic correlations between larval and juvenile stages, implying genetic independence of life-history traits between life-stages. We suggest two possible scenarios for the maintenance of genetic polymorphism in the early life-history strategy of C. gigas.

Animals↗
PubMed2003

Association of muscarinic m1 receptor genetic polymorphisms with psychiatric symptoms and cognitive function in schizophrenic patients.

OBJECTIVE: The cholinergic system is important in the search for the pathophysiology of schizophrenia due to its role in cognitive function, interaction with the dopamine system in brain regions relevant to schizophrenia, side effects of antipsychotic medication and potential antipsychotic effect of muscarinic receptor antagonists. This study investigated the association of type I muscarinic receptor (CHRM1) genetic polymorphisms with the clinical characteristics of chronic schizophrenic inpatients. METHODS: We determined the genotype of CHRM1 genetic polymorphisms in 243 schizophrenic patients hospitalized in chronic care wards. Psychotic symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS), and cognitive function was assessed using the Folstein Mini-Mental Status Examination (MMSE) test. Sixty of the 243 subjects also completed the Wisconsin Card Sorting Test (WCST). RESULTS: There was a significant difference in the number of correct responses and the percentage of perseverative errors in the WCST in the CHRM1 C267A genotype group of schizophrenia patients. There was no significant association between age at onset, chlorpromazine equivalents, BPRS scores, MMSE or schizophrenia per se in patients with the CHRM1 C267A genotype. The full exon of the CHRM1 gene was screened out with single-strand conformation polymorphism, and 2 single nucleotide polymorphisms (C267A and C1353T) were identified in our patients and control subjects. These 2 single nucleotide polymorphisms were linked together without exception. CONCLUSION: This study demonstrated that in schizophrenic patients, the heterozygote group of CHRM1 C267A polymorphism (267C/A) had more correct responses and less perseverative errors on the WCST performance than the 267C/C homozygote group, implicating that this polymorphism may be related to prefrontal cortical function. Our results also suggested that the C267A polymorphism plays no major role in the susceptibility to and clinical manifestations of schizophrenia.

Adolescent↗
PubMed2004

Genetic polymorphism of p53 and XRCC1 in cervical intraepithelial neoplasm in Taiwanese women.

BACKGROUND AND PURPOSE: Many epidemiological studies have investigated the relationship between p53 codon 72 polymorphism and cervical cancer risk, but the findings are still conflicting. In contrast, data are lacking on the relationship between XRCC1 polymorphism and cervical neoplasm risk. This community-based nested case-control study examined the association between genetic polymorphisms of p53 codon 72 and XRCC1 codons 194, 280, and 399 and cervical intraepithelial neoplasm (CIN) susceptibility in Taiwanese women. METHODS: Women living in Chiayi City, located in southwestern Taiwan, who had received Papanicolau (Pap) smear screening between October 1999 and December 2000 (n = 32,466) were included. Potential cases were women having lesions with cervical intraepithelial neoplasm II (CIN2) and over (> or = CIN2) reconfirmed by cervical biopsy. Potential controls (case:control = 1:2) were age matched (+/- 2 years) and residency matched women who had normal Pap smears. DNA samples were extracted from peripheral blood specimens and genetic polymorphisms of p53 and XRCC1 were determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: In total, 100 cases [97 high-grade squamous intraepithelial lesion (HSIL) and 3 invasive cancer] and 196 controls had complete demographic and clinical questionnaire data and data of analysis of XRCC1 polymorphism, whereas only 99 cases and 193 controls had complete data for p53 polymorphism. The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different. The frequency of arg/arg, arg/gln, and gln/gln in XRCC1 codon 399 in cases was 54% (54/100), 38% (38/100), and 8% (8/100) and in controls was 58% (114/196), 37% (73/196), and 5% (9/196), respectively, which was not significantly different. No associations were found between XRCC1 codon 194 and 280 genotypes and HSIL risk. The joint effect of p53 and XRCC1 polymorphisms remained insignificant. CONCLUSIONS: Our data suggest that p53 codon 72 and XRRC1 codon 194, 280 and 399 genotypes do not influence CIN risk in the Taiwanese population.

Adult↗
PubMed1997

Association of apolipoprotein genetic polymorphisms with plasma cholesterol in a Japanese rural population. The Shibata Study.

The association between apolipoprotein (apo) genetic polymorphisms and lipid phenotypes remains to be determined because such studies have reported contradictory results. We have measured plasma total cholesterol (TC) and HDL cholesterol (HDL-C) in a cross-sectional sample of 1328 (462 men and 866 women) Japanese (aged 40 to 80 years) and analyzed their DNA for the following genotypes: apoA1-C3 Msp I and Sst I sites; apoB signal peptide insertion/deletion, Xba I site and 3' variable number of tandem repeats (VNTR); and apoE. Using multivariate analyses (ANOVA) we found that (1) the polymorphisms of apoA1-C3 and apoB genes are not significantly associated with TC or HDL-C and (2) the polymorphism of the apoE gene is significantly related with TC and the TC:HDL-C ratio. The epsilon 2 carriers have lower levels of TC and a lower TC:HDL-C ratio, epsilon 3 carriers have intermediate levels, and epsilon 4 carriers have higher levels. These findings held whether sexes were analyzed separately or together. Although an opposite trend in HDL-C levels was observed, it did not reach the level of statistical significance. Multiple regression analyses have shown that apoE polymorphism accounts for about 2.3% of the variation in TC and TC:HDL-C ratio irrespective of sex. When the subjects are divided into two groups according to their age (< or = 59 and > or = 60 years old), the effect of apoE alleles on serum cholesterols appears to be diluted in the younger age group whereas it appears to be accentuated in the older group for both sexes. Our findings suggest that among the apo genetic polymorphisms examined, the apoE gene may be considered as a possible candidate for the "high-risk" strategy of atherosclerosis prevention in the Japanese population.

Adult↗
PubMed1985

The significance of over- and underdominance for the maintenance of genetic polymorphisms. I. Underdominance and stability.

It is pointed out that the standard selection models in population genetics all require some form of heterozygote advantage in fitness in order to guarantee the maintenance or stability of genetic polymorphisms. Even more recent results demonstrating the existence of stable two-locus polymorphisms with marginal underdominance at both loci are based on certain epistatically acting heterosis assumptions. This raises the question as to whether heterozygote advantage in fitness is indeed a generally valid principle of maintaining polymorphisms. To avoid ambiguity in definition of heterozygote advantage (overdominance) as it appears in multiallele or multilocus systems, a one-locus-two-allele model is considered. This model allows for sexually asymmetric selection and random mating. It is shown that the model produces globally stable polymorphisms exhibiting underdominance in fitness for a considerable and biologically reasonable range of selection values. Having thus properly refuted the general validity of the common overdominance principle, a modified version is suggested which covers the classical viability selection model and its extension to arbitrary, sexually asymmetric viability and fertility selection. This modified overdominance principle is based on the notion of fractional fitnesses and relates protectedness of biallelic polymorphisms to the extent to which each genotype reproduces its own type. The fact that the model treated displays frequency dependent fitnesses which may change in ranking while approaching equilibrium is discussed in relation to problems of the evolution of overdominance and underdominance.

Animals↗
PubMed2002

[Studies of genetic polymorphisms of ADH2 and ALDH2 among the Han population in Luoyang China].

In order to investigate genetic polymorphisms of ADH2 and ALDH2 among the Han population in Luoyang City,portions of exon 3 of ADH2 and exon 12 of ALDH gene were amplified by using polymerase chain reaction. The amplified products were electrophoresed on 10% undenatured vertical polyacrylamide gels and stained with argentine. Frequencies of ADH2*1 and ADH2*2 alleles are 42.86% and 57.14%. Frequencies of three genotypes of ADH2 are 22.86%,40.00% and 37.14%,respectively. Frequencies of ALDH2*1 and ALDH2*2 alleles are 85.24% and 14.76%. Genotype frequencies of ALDH2 loci are 71.43%,27.62% and 0.95%,respectively. Genetic polymorphisms of ADH2 and ALDH2 among the Han population in Luoyang City are different from those among Taiwanese and Shanghainese. Frequency of ALDH2*1/*1 in Luoyang people is higher than those in Shanghai and Taiwan. Therefore,there is a higher resistance to alcohol drinking in the Han population in Luoyang.

English Abstract↗
PubMed2004

Prognosis of young ischemic stroke in Taiwan: impact of prothrombotic genetic polymorphisms.

We investigated the effects of genetic factors on the prognosis of cerebral infarction in young adults in Taiwan. Because ischemic stroke with arterial occlusion or undetermined etiology is more likely to be related to a genetic prothrombotic state, 231 patients younger than 50 years (mean age 44.6 years, range 25 to 49 years) with acute ischemic stroke due to large artery atherosclerosis (n=90), small artery occlusion (n=114) or undetermined cause (n=27) were recruited and prospectively followed up for pre-determined outcome. On each patient, we screened the PlA1/PlA2 polymorphism of the platelet glycoprotein IIIa gene, 4G/5G polymorphism of the plasminogen activator inhibitor-1 gene, G10976A polymorphism of the factor VII gene, C677T polymorphism of the methylenetetrahydrofolate reductase gene, and 27 base-pair repeat polymorphism of the endothelial nitric oxide synthase gene. End points were the composite outcome events of stroke, myocardial infarction, and death from all causes. During a mean duration follow-up of 29 months, composite outcome events occurred in 33 patients. There was a higher annual incidence rate of composite outcome events during the first year (9.1%, 95% CI 5.9-13.9%) than in the subsequent 2 years (2.6%, 95% CI 1.2-5.6%, p=0.038). None of the genetic polymorphism was associated with the composite outcome events. Past history of coronary artery disease or cerebrovascular disease was the only independent predictor of the composite outcome events (HR 3.71, 95% CI 1.69-8.14, p=0.001) at the Cox regression analysis. Our data indicate that the prothrombotic genetic polymorphisms do not have a significant influence on the prognosis in young ischemic stroke due to arterial occlusion or undetermined causes in Taiwan.

Adult↗
PubMed2005

Influence of genetic polymorphisms of styrene-metabolizing enzymes and smoking habits on levels of urinary metabolites after occupational exposure to styrene.

Here we evaluate the influence of individual genetic polymorphisms of drug-metabolizing enzymes as well as body mass index (BMI) and lifestyle (smoking, alcohol consumption) on urinary metabolites after occupational exposure to styrene. Seventy-three workers exposed to styrene in a reinforced-plastics workplace were studied. The personal styrene exposure in the air and the urinary styrene metabolites mandelic acid and phenylglyoxylic acid were measured. The subjects' genetic polymorphisms in the genes that encode the styrene-metabolizing enzymes CYP2E1, CYP2B6, EPHX1, GSTM1, GSTT1 and GSTP1 were determined. Neither genotype nor lifestyle significantly affected urinary metabolites. There was, however, an interaction between the CYP2E1 genotype and smoking. Among non-smokers, urinary styrene metabolites were significantly decreased in subjects with c1/c1 alleles of CYP2E1 as compared with those with the c1/c2 genotype. There was no significant difference in urinary metabolites among smokers. When the combined influence of the CYP2B6 genotype and the predicted activity of EPHX1 were examined, urinary metabolites in subjects with low enzyme activity were lower than in those with medium or high activity after high styrene exposure (>or=50 ppm). The results suggest that genetic susceptibility and lifestyle should be considered in biological monitoring of exposure to styrene.

Adult↗
PubMed2005

Genotoxic effects in a population of nurses handling antineoplastic drugs, and relationship with genetic polymorphisms in DNA repair enzymes.

BACKGROUND: Concern about the genotoxic risk associated with chronic handling of antineoplastic drugs has increased, and usual safety practices may not avoid exposure. METHODS: Comet assay and MN test were performed on 30 oncology nurses and 22 controls. Genetic polymorphisms of XRCC1, XRCC3, and APE1 genes were determined by PCR-RFLP. RESULTS: Data obtained showed increased cytogenetic and DNA damage in the exposed group, although statistical significance was only reached in the comet assay. Significant differences in TL were observed for carriers of the variant alleles of every gene analyzed. However, no significant effect was detected in the MN test. CONCLUSIONS: Evidence that the present handling practices of antineoplastic drugs in some Portuguese hospitals are not enough to prevent exposure are provided. Present data suggest that genetic polymorphisms in the studied DNA repair enzymes may influence the individual susceptibility to DNA damage related to chronic handling of antineoplastic drugs.

Adult↗
PubMed2005

Genetic polymorphisms and the effect of cigarette smoking in the comet assay.

A potential genotoxic effect of cigarette smoking has repeatedly been investigated with the comet assay (alkaline single cell gel electrophoresis) and conflicting results have been reported. Besides differences in the methodology and the study design used, genetic differences between the subjects investigated might contribute to the variability of test results. Considering genetic polymorphisms of genes involved in metabolism or DNA repair has led to a better discrimination of smoking-related genotoxic effects in some cases but also led to discrepant results. We therefore evaluated our baseline comet assay effects obtained for nonsmokers and smokers in relation to selected genetic polymorphisms. Our study group comprised 52 nonsmokers and 51 smokers who were strictly selected to exclude potential confounding factors. We chose polymorphisms in the genes GSTM1 and CYP1A1 (Ile462Val) because they take part in the metabolism of genotoxins contained in tobacco smoke. In a subgroup of 32 nonsmokers and 31 smokers we also studied polymorphisms in XPD (Lys751Gln), XRCC1 (Arg399Gln) and XRCC3 (Thr241Val) because they are part of DNA repair pathways involved in the repair of tobacco-related DNA damage. Freshly collected peripheral whole blood samples were tested in the alkaline (pH > 13) comet assay. In all experiments a reference standard (untreated V79 cells) was included to correct for assay variability. An independent second evaluation was carried out for all experiments. None of these approaches revealed a significant difference between nonsmokers and smokers.

Comet Assay↗
PubMed1998

A genetic polymorphism of MAO-B modifies the association of cigarette smoking and Parkinson's disease.

In a population-based case-control study, we found a reversal of the association of cigarette smoking with Parkinson's disease (PD) in relation to the monoamine oxidase B intron 13 genetic polymorphism. A reduced PD risk related to pack-years of smoking was detected for persons with the G allele, whereas an opposite effect was found among persons with the A allele. These results indicate an unexplained interaction between cigarette smoking and this genetic polymorphism.

Adult↗
PubMed2000

[N-acetyltransferase genetic polymorphism and its role in the development of neoplastic disease].

N-acetyltransferases are the enzymes present in the cells of most mammal species. In human cells, the activity of two N-acetyltransferases, known as NAT1 and NAT2, is expressed. These enzymes are coded by two different genes: NAT1 and NAT2. Gene NAT1 is expressed in the cells of the majority of tissues and organs, whereas gene NAT2 only in the liver and intestine. Acetylation polymorphism and resultant division into the fast and free acetylators is caused by the occurrence of gene wild allele NAT2 and its mutated forms. A given person shows the fast acetylation phenotype if at least one allele NAT2 is wild. The presence of mutation in both alleles NAT2 is manifested by a free acetylation phenotype. It was indicated that gene NAT1 is also polymorphic, and together with its wild form, the mutated forms are also observed. Genetic polymorphism of NAT1 and NAT2 has serious pharmacological and toxicological consequences. Epidemiological studies show that the free acetylation phenotypes are more susceptible to bladder cancer than the fast ones if they smoke or work under exposure to bicyclic aromatic amines. It has also been evidenced that the fast acetylation phenotypes show enhanced risk of large intestine cancer in conditions of environmental and occupational exposure to heterocyclic amines. It has not as yet been found out whether the acetylation status may be linked with the increased risk of lung cancer.

Alleles↗
PubMed1998

Chromosome geometry and intraspecific genetic polymorphism in Gram-positive bacteria revealed by pulsed-field gel electrophoresis.

Pulsed-field gel electrophoresis (PFGE) proved to be a powerful approach to study bacterial genomics. The genome structure and genetic polymorphism of Gram-positive bacteria from the high G+C (Streptomyces) and low G+C (Streptococcus) groups have been studied. PFGE allowed the estimation of the size of their genome at about 8 Mbp and 1.8 Mbp, respectively, and to get an insight into their chromosome geometry. Thus, physical mapping of the genome of wild-type Streptomyces ambofaciens strains revealed the linearity of the 8 Mbp chromosomal DNA and its typical invertron structure, while the 1.8 Mbp chromosome of Streptococcus thermophilus was shown to be circular. These findings disproved the long-standing idea of universality of bacterial chromosome circularity. In addition, strains belonging to the species S. ambofaciens and S. thermophilus allowed us to characterize the genetic polymorphism at the intraspecific level. Within the S. thermophilus species, comparison of the physical maps showed a relative conservation of gene order as well as restriction sites along the chromosome. In contrast, variable loci were characterized that revealed localized genome rearrangements. The most spectacular of these corresponded to horizontal gene transfer events of sequences. In S. ambofaciens, the physical maps of three isolates pointed to the conservation of the genetic organization. However, a strong polymorphism was observed in the terminal regions of the linear chromosomal DNA. Previous PFGE studies in S. ambofaciens gave proof of a high structural instability of a limited region of the chromosome called unstable region (i.e., DNA rearrangements such as deletions and amplifications). These intraclonal rearrangements create an impressive intraspecific polymorphism of genome size and shape (linear or circular). In both organisms, the DNA rearrangements are restricted to particular regions of the chromosome.

Chromosomes, Bacterial↗
PubMed2001

Genetic polymorphism at the glutathione S-transferase (GST) P1 locus is a breast cancer risk modifier.

The isolation of full-length cDNAs of naturally occurring GSTP1 gene variants, and the demonstration that these alleles are distributed in the normal population, have provided conclusive evidence that the human GSTP1 gene locus is polymorphic and that specific GSTP1 alleles may be associated with different risk for cancers or other diseases. Recent data have indicated that the different GSTP1 alleles encode proteins with different enzymatic activities against carcinogens. In this case-control study, we examined the effect of the GSTP1 genetic polymorphism and its interaction with other factors to determine breast cancer risk. GSTP1 and GSTM1 genotypes of 220 breast cancer patients and 196 controls, all residents of western France, were examined. Data on menopausal status and family cancer history were obtained from 195 patients and 147 controls. Exons 5 and 6 of the GSTP1 gene, which contain the polymorphic nucleotide transitions, were analyzed by DNA polymerase chain reaction-restriction fragment length polymorphism to distinguish between the GSTP1 alleles. In the control population, GSTP1 allelic frequencies were 64.3%, 26.0% and 9.7%, respectively, for GSTP1*A, GSTP1*B and GSTP1*C. In the breast cancer patients, the frequencies were 67.9% for GSTP1*A, 26.8% for GSTP1*B and 5.3% for GSTP1*C. In multivariate analysis, breast cancer risk increased by 7.7-fold (p < 0.001) in women with a family history of cancers and 2.18-fold (p = 0.026) in non-GSTP1*C individuals. GSTM1 genotypes did not emerge as risk factor. Our results show that in addition to well-known risk factors, in particular, a family history of cancer, GSTP1 allelopolymorphism is a significant modifier of breast cancer risk. The results also suggest a protective role against breast cancer for the GSTP1*C allele.

Adult↗
PubMed1990

Genetic polymorphisms of Q region genes from wild-derived mice: implications for Q region evolution.

Both serological and DNA sequence analyses were performed to determine the extent of genetic polymorphism in Q region genes. A panel of Qa-2-specific monoclonal antibodies (mAbs) was tested on 35 wild-derived and inbred mouse strains. Members of this reagent panel recognize multiple and distinct epitopes on the Qa-2-bearing molecule(s). Although quantitative variations in Qa-2 levels were observed, no structural polymorphisms were detected. All strains were either entirely positive or entirely negative with the complete set of reagents. Moreover, cell surface Qa-2 expression was not significantly affected by differences in age or sex of the mouse or cell cycle status. To confirm this apparent lack of genetic polymorphism, the polymerase chain reaction (PCR) technique was used to amplify a portion of the 3' end of the Q region genes, Q4 to Q9, from several independent wild-derived strains of mice. Sequence analysis of the amplified material revealed very little evidence of nucleotide divergence. All strains tested had a Q even DNA sequence identical to that of Q6/Q8 in the B10 strain. Likewise, all tested strains had a Q odd DNA sequence identical to Q7/Q9 in the B10 strain. Two strains showed additional Q even sequences, while all strains tested possessed additional Q odd sequences. The observed lack of polymorphism suggests that the Q genes have evolved in a different manner from H-2K and H-2D. Moreover, duplications of these genes appear to have arisen prior to nucleotide sequence divergence.

Aging↗
PubMed2006

Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma.

Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma. Hepatotoxicity and bone marrow suppression often limit its use, however. The objective of this study was to determine the genetic polymorphisms associated with the hepatotoxicity and elimination of methotrexate. Genetic polymorphisms of glutathione S-transferase (GST) genes including GSTT1 positive/null, GSTM1 positive/null, and GSTP1 A313G, and genes for reduced folate carrier 1 G80A (RFC1 G80A), methylenetetrahydrofolate reductase C677T (MTHFR C677T), and breast cancer resistant protein C421A (BCRP C421A) were determined for 26 patients by the polymerase chain reaction (PCR) method or by direct sequencing. A high frequency of hepatotoxicity (P = 0.035) was observed for patients with GSTM1 positive and RFC1 AA(80), and serum concentrations of methotrexate 48 h after the start of infusion were higher for patients with the TT(677) genotype of MTHFR (P = 0.028). In conclusion, GSTM1 positive/null and RFC1 G80A polymorphisms could be predictors for hepatotoxicity, and the MTHFR C677T polymorphism is associated with elimination of methotrexate.

Adolescent↗
PubMed1982

Influence of double genetic polymorphism on response to sulfamethazine.

Combined effects of a double genetic polymorphism on sulfamethazine-induced changes in erythrocyte-reduced glutathione (GSH) concentration were investigated in 16 healthy Ghanaian men. The subjects were divided into four subgroups on the basis of their glucose-6-phosphate dehydrogenase (G-6-PD) activity levels and acetylator phenotypes. Each received a single oral dose of sulfamethazine (1.5 gm). Erythrocyte concentration of GSH and plasma concentrations of drug were determined in samples taken at specific times after dosing. Sulfamethazine treatment induced a decrease in erythrocyte GSH concentration in all subjects. The degree of exposure to sulfamethazine was greater in slow acetylators, as evidenced by higher plasma concentrations, longer half-lifes, and greater area under the plasma concentration-time curves. The greatest decrease in GSH concentration occurred in subjects who where both G-6-PD deficient and phenotypically slow acetylators. In these subjects the effect of the double genetic defect was approximately additive. Drug-induced hemolysis is associated with a low erythrocyte GSH concentration. Our data suggest that slow acetylator status is likely to increase susceptibility to hemolysis in G-6-PD-deficient individuals exposed to potentially hemolytic arylamines.

Acetylation↗
PubMed1997

Genetic polymorphism of cytochrome P-4502E1 and mitochondrial aldehyde dehydrogenase in a Korean population.

Mitochondrial aldehyde dehydrogenase (ALDH2) is mainly responsible for the oxidation of acetaldehyde generated during alcohol oxidation in vivo. Cytochrome P-4502E1 (CYP2E1), a liver microsomal enzyme, also metabolizes acetaldehyde and ethanol. Genetic polymorphism of ALDH2 and CYP2E1 was investigated among 481 Korean adults. A new restriction fragment-length polymorphism method was developed to determine the genotype of the ALDH2 alleles. This method proved to be simpler and faster than the hybridization method using allele-specific oligonucleotide probes and polymerase chain reaction-directed mutagenesis. The allele frequencies of ALDH2(1) and ALDH2(2) were 0.840 and 0.160, respectively. This allele frequency of ALDH2(2) is less than in Japanese people. Genetic polymorphism of CYP2E1 was investigated using polymerase chain reaction and restriction fragment-length polymorphism. The estimated allele frequencies for c1 and c2 were 0.808 and 0.192.

Adult↗