Environmental lead exposure, catalase gene, and markers of antioxidant and oxidative stress relation to hypertension: an analysis based on the EGAT study.

Lead has been linked to the development of hypertension via oxidative stress. Catalase plays an important role in the disposal of hydrogen peroxide in erythrocyte and its activity was determined by CAT gene. The aims of this study were to investigate (1) the association between blood levels of antioxidant markers such as catalase, superoxide dismutase, glutathione, glutathione peroxidase, oxidative stress-marker (malondialdehyde), and blood lead level and (2) the influence of genetic polymorphism of CAT gene (rs769217) on change in blood pressure in general population of EGAT study project. This is a cross-sectional study of 332 normotensive, 432 prehypertensive, and 222 hypertensive male subjects. Hypertensive subjects had significantly higher blood lead level (5.28 µg/dL) compared to normotensive (4.41 µg/dL) and prehypertensive (4.55 µg/dL) subjects (P < 0.05). These significant findings are also found in MDA levels. Moreover, individuals with TT genotype in hypertensive group had significantly higher blood lead and MDA levels (6.06 µg/dL and 9.67 µmol/L) than those with CC genotype (5.32 µg/dL and 8.31 µmol/L, P < 0.05). Our findings suggested that decreased blood catalase activity in this polymorphism together with low level lead exposure induced lipid peroxidation may be responsible for hypertension.

Association between serum homocysteine, folate and B12 concentration with coronary artery disease in Thai patients.

BACKGROUND: Hyperhomocysteinemia, associated with low folate and low B12 levels, is known to be an independent risk factor for atherosclerosis. Only a few available data has been demonstrated in Thai patients. OBJECTIVE: To evaluate serum fasting homocysteine, folate and B12 levels whether to see they are associated with coronary artery disease (CAD). METHOD AND RESULT: Three hundred and one consecutive suspected CAD patients who underwent coronary angiography at the Police General Hospital were studied. The mean age of the patients, 195 males and 106 females, was 63.0 +/- 10.0 year (range 39-85). A total of 218 patients were angiographically demonstrated as having CAD. The mean serum homocysteine level of CAD patients had a non significant higher level than those of 83 non CAD patients: 11.4 +/- 6.2 vs 10.2 +/- 4.2 umol/L, p = 0.06. Means of folate and B12 level in the CAD patients and non CAD patients were 6.6 +/- 4.6 vs 7.0 +/- 4.3 nmol/L, p = 0.49 and 650.9 +/- 415.4 vs 613.3 +/- 443.2 pmol/L, p = 0.56 respectively. No significant correlations were found between homocysteine with folate and B12 levels. Logistic regression analysis showed a significant association between homocysteine and CAD with OR = 1.08 (95%CI, 1.01-1.16), p = 0.03 after being adjusted for age, sex, DM, HT history of hyperlipidemia, smoking, BMI, folate and B12 levels. No significant association between homocysteine level with the number of coronary vessel stenosis, age, BMI, DM, HT smoking and history of hyperlipidemia was observed in the present study. CONCLUSION: Hyperhomocyteinemia, but not folate and B12 levels, may be an independent risk factor for coronary artery disease in Thai patients.

Genetic variations of glutathione s-transferase influence on blood cadmium concentration.

The glutathione S-transferases (GSTs) are involved in biotransformation and detoxification of cadmium (Cd). Genetic polymorphisms in these genes may lead to interindividual variation in Cd susceptibility. The objective of this study was to assess the association of GSTs (GSTT1, GSTM1, and GSTP1 Val105Ile) polymorphisms with blood Cd concentrations in a nonoccupationally exposed population. The 370 blood samples were analyzed for Cd concentration and polymorphisms in GSTs genes. Geometric mean of blood Cd among this population was 0.46 ± 0.02 µg/L (with 95% CI; 0.43-0.49 µg/L). Blood Cd concentrations in subjects carrying GSTP1 Val/Val genotype were significantly higher than those with Ile/Ile and Ile/Val genotypes. No significant differences in blood Cd concentrations among individual with gene deletions of GSTT1 and GSTM1 were observed. GSTP1/GSTT1 and GSTP1/GSTM1 combinations showed significantly associated with increase in blood Cd levels. This study indicated that polymorphisms of GSTP1 combined with GSTT1 and/or GSTM1 deletion are likely to influence on individual susceptibility to cadmium toxicity.