GSTM1和T1基因多态性与AFT暴露和肝癌

AIM To explore the relationship between the level of aflatoxin-human serum albumin adducts and polymorphisms of glutathione S-transferase (GST) M1 and T1 and primary liver cancer (PLC).METHODS AFT-albumin adducts were measured by sandwich enzyme-linked immunosorbent assay (ELISA) and genotypes of GST M1 and T1 were determined by PCR.RESULTS Compared with those with non-null genotype of both GST T1 and M1, the odds ratio of developing PLC for those with null genotype of both GST T1 and M1 was 3.11 (95% confidence interval: 1.01-9.98; P=0.029). There was a dose-response relationship between serum level of AFT-albumin adducts and risk of PLC (χ2trend=15.42, P=0.0001). By combined genotype of GST T1 and M1, persons with null genotype of GST T1 and M1 were more likely to have higher AFT-albumin adduct level than those with other genotypes of GST T1 and M1 (F=4.57, P＜0.005). The biological gradients between serum AFT-albumin adducts level and PLC risk were observed to determine whether the persons were of null genotype of GST T1 or M1 or not. The levels of AFT-albumin adduct in Haimen residents in 1992 and 1996 were decreased significantly as against 1987 (F=6.35, P＜0.005).CONCLUSION Exposure to aflatoxin may still be one of risk factors leading to PLC endemic in Haimen population and those with null genotype of GST T1 and M1 may be at greater risk of developing PLC once they are exposed to aflatoxin.

Objective To analyze the relationship between polymorphism at the Apolipoprotein AI (Apo AI) gene and the risk for coronary artery disease. Methods A total of 107 patients (mean age 56 ± 11 years) diagnosed as having stable angina pectoris (SAP) (23 cases), unstable angina pectoris (UAP)(23 cases) or myocardial infarction (MI) (61 cases)were prospectively evaluated. DNA was obtained from the 107 patients and 50 controls. In order to determine the Apo AI genotypes at two polymorphic sites (G/A at -75 bp, and C/T at +83 bp), DNA was PCR amplified and digested with MspI. Results The frequency of carriers of the rare allele at the - 75 bp site (M1-) was 0.49 in cases and 0.30 in controls ( P＜ 0.05). The frequencies of the M 1 - allele among patients with SAP, UAP, MI and controls were 0. 37 (vs. Controls, P ＞ 0.05), 0. 54 (vs. Controls, P ＜0.05), 0.52 (vs. Controls, P＜ 0.05) and 0.30, respectively. The frequencies for carriers of the rare allele at the + 83bp polymorphism (M2) were observed among patients with SAP (0.09, vs. Controls, P ＞0.05), UAP (0. 11, vs. Controls, P ＞ 0.05) or MI (0.12, vs. Controls, P ＞ 0.05) and controls (0. 12).There was an slightly increase in the frequency of the M1 - allele in patients with SAP to UAP or MI (0.37vs. 0.54 vs. 0.52; all P ＞ 0.05) and M1 polymorphism as a risk factor for CAD (OR=3.74, P ＜0.05). In the + 83bp polymorphism there was no difference in the allelelic frequencies in cases and controls (0. 11 vs. 0. 12; P ＞ 0.05). There was no significant difference in the frequency of the M2- allele in patients with SAP to UAP or MI (0.09 vs. 0.11 vs.0. 12; all P ＞ 0. 05) and M2 polymorphism not as a factor for CAD ( OR = 0. 80, P ＞ 0. 05) Plasma lipoprotein values in patients with the allele M1 - and M2 - had no different levels than those homozygous for the M1+ andM2+ (P＞ 0.05). Conclusion M1polymorphism (M1 - ) may be as a risk factor for CAD and M2 polymorphism (M2 - ) not as a factor for CAD in Chinese Xinjiang Uygur and Han population.