A study of oxidative stress, antioxidant status and lipid profile in diabetic patient in the western region of Nepal.

AIMS AND OBJECTIVES: Diabetes mellitus (DM) is often termed as a disease of premature aging. Several studies have indicated lopsided redox balance due to pro oxidant environment as one of the important etiological factors. Some recent researches also indicate a causal relationship with oxidative stress (OS). So far, no study has been undertaken on this aspect in Nepali populations. We, therefore, aimed this maiden study in Nepali population to examine redox balance by measuring OS and antioxidant status along with lipid profile in 37 patients of DM type- 2 and 30 matched normal subjects. METHODOLOGY: Thirty seven patients of DM type-2 without any complications (mean age= 57.6+/- 10.6 years) and 30 normal subjects (mean age= 55.8 +/- 14.8 years) were included in this study. Body Mass Index (BMI) and Waist/Hip (W/H) ratio were measured. Fasting blood sample was collected for the analysis of total antioxidant activity (TAA), plasma and urinary thiobarbituric acid reactive substances (TBARS) and lipid profile by standard procedures in both the groups. The statistical analysis was done with SPSS 10 version. RESULTS: Total cholesterol, triglyceride, VLDL-cholesterol, LDL-cholesterol, plasma and urinary TBARS were significantly raised whereas, plasma TAA was significantly reduced in DM type-2 patients as compared to controls. The comparison of old and fresh cases revealed that though TAA was lower and PTBARS and UTBARS were higher in patients but did not attain the level of significance. W/H ratio is significantly higher in patients compared to normal subjects. But, no significant correlation of BMI and W/H with lipid profile is observed in both control and patients. CONCLUSION: Oxidative stress is raised in type 2 DM patients. This along with deranged lipid profile and decreased antioxidant status could be the risk factors in the development of complications associated with DM.

Cigarette smoke induced oxidative insult in local population of Pokhara.

OBJECTIVES: To assess the effect of cigarette smoking on lipid peroxidation induced oxidative stress, antioxidants, uric acid and blood sugar in normal subjects. METHODS: The study included 61 normal subjects with regular smoking habit and 57 never-smokers normal subjects matched in respect to socio-economic status, age and BMI. Information regarding smoking habit and other personal details were collected by oral questionnaire. Total antioxidant activity (TAA), reduced glutathione (GSH), alpha-tocopherol (alpha-T), ascorbic acid (AA), uric acid (UA), plasma and urinary thiobarbituric acid reactive substances (TBARS), fasting blood sugar (FBS) and urinary creatinine (Cr) were estimated by standard procedures in both the groups. Ferric Reducing Antioxidant Power (FRAP) procedure is used to estimate TAA which measures total dietary antioxidants. Statistical analysis was done with SPSS version 10. RESULTS: The mean pack years smoked by smokers was 14.4 +/- 15.8. The plasma TBARS level in smokers and never-smokers was 2.6 +/- 0.8 and 2.5 +/- 0.6 micromol/L respectively. The respective figure for urinary TBARS level was 4.6 +/- 2.7 and 3.7 +/- 1.4 micromol/gmCr. Smokers did not show any significant difference from never-smokers with respect to GSH, alpha-T, AA, plasma TBARS and FBS. However, the smokers had significantly lower levels of TAA (p<0.05) and raised level of urinary TBARS (p<0.05) and uric acid (p<0.01) as compared to never-smokers. CONCLUSION: Our study suggests that smoking induces mild lipid peroxidation but the body is able to compensate for it by removing its adducts. Importantly it also indicates enhanced oxidation of purines which are essential components of both DNA and RNA. Dietary antioxidants are consumed to scavenge free radicals (FR) and other reactive species (RS) in smoke. Female smokers are more prone to oxidative insult than male smokers. In summary RS present in smoke induce mild lipid peroxidation but are not the major contributors of redox imbalance in smoke induced toxicity in the selected subjects.