Aspirin esterases in North-West Indians: the influence of age and nutrition.

OBJECTIVE: To determine the activity of aspirin esterases in North-West Indian population and to find the effect of age and nutrition on it. SUBJECTS, MATERIAL AND METHODS: The serum albumin, plasma cholinesterase (PChE), aspirin esterase (ASPES) and phenyl acetate esterase (PAE) were determined in 175 subjects: young (< 40 years) and healthy (BMI > 19) = 74; elderly (> 50 years) and healthy (BMI > 19) = 32; young (< 40 years) and emaciated (BMI < 19) = 44; elderly (> 50 years) and emaciated (BMI < 19) = 25). RESULTS: The serum albumin levels significantly decreased with increase in age (r = -0.384, p < 0.01) and with decrease in body mass index (r = 0.457, p < 0.01). When the activity of esterases in four groups was compared, the PAE activity was not found to be affected by age or nutrition and the ASPES and PChE activity were significantly lower only in elderly emaciated (p < 0.01). CONCLUSION: As elderly emaciated have decreased serum albumin, ASPES and PChE activity, they may need a lower dose of aspirin to achieve the desired antiplatelet and analgesic effect. The young emaciated subjects, in spite of their lower serum albumin levels, may not require a lower dose of aspirin.

Paraoxonase (PON1) polymorphism & its relation with lipids in north west Indian Punjabis.

We investigated 190 healthy, unrelated and randomly selected, north-west Indian Punjabis (M:102; F:88) for paraoxonase (PON1) polymorphism by dual substrate method and also determined lipid variables i.e., total cholesterol (TC), high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL) and triglycerides (TG) in them to determine any relationship between PON1 activity, PON1 phenotypes and lipids. The basal plasma paraoxonase (PON) activity, and PON activity in presence of 1 Mol NaCl (salt activated paraoxonase i.e., SAP) were estimated by using paraoxon as substrate whereas the, phenyl acetate esterase (A) activity was estimated by using phenylacetate as substrate. Based on the ratio of SAP/A activity, three distinct phenotypes of PON1 could be determined with gene frequencies of PON*A (low activity) and PON*B (high activity) allele being 0.847 and 0.153 respectively. In the whole population on partial correlation after normalising the variables and after adjusting the lipids for age and body mass index (BMI), a significant negative correlation was observed between SAP/A ratio and TC (r = -0.290; P < 0.01) and LDL (r = -0.154; P < 0.05). However, on analysis of covariance (ANCOVA) after normalizing the lipid variables and adjusting these for age and body mass index (BMI), no significant difference could be observed in lipid profile of these three phenotypes. The lack of a significant relationship between lipids and PON1 phenotypes, suggests that PON phenotype does not significantly influence the lipid profile in north-west Indian Punjabis. However, a significant negative correlation between the PON activity and TC and LDL suggests that low PON activity could be a risk factor for atherosclerosis in these subjects.

Red cell acetyl cholinesterase and plasma cholinesterase activity and genetic variants of plasma cholinesterase in northwest Indian adults.

The plasma cholinesterase (PChE) and red cell acetyl cholinesterase (AChE) activities are indicators of exposure to organophosphates. We studied their distribution in unexposed Northwest Indian adults by measuring them in 120 men and 111 women by Ellman's and Kalow's method, respectively. We also determined genetic variability of plasma cholinesterase in 193 subjects (male = 111, female = 82). The mean +/- (SD) AChE levels in population, men and women, were 34.97 +/- 13.66, 35.05 +/- 12.42, 34.88 +/- 14.89 nmol/mg Hb/min, whereas PChE was 0.448 +/- 0.173, 0.435 +/- 0.163, 0.462 +/- 0.183 ku/l, respectively. When compared for sex, no significant difference could be found for red cell AChE and PChE activity. However, on 2-way analysis of variance (ANOVA) adjusted for age classification, the levels of both AChE and PChE were significantly higher in groups above the age of 30 years as compared to below 30 years (t = 3.08, p < 0.01, t = 2.82, p < 0.05), respectively. Seven genetic variants of PChE could be detected in males, whereas in females 6 genetic variants were found.