Adenosine deaminase (ADA) is an enzyme of purine salvage pathway and has two important isoenzymes ADA1 and ADA2. The activity of ADA has been changed in diseases characterized by altered cell-mediated immunity. It was observed that total serum ADA activity was decreased during normal pregnancy compared with non-pregnant women. However, total serum ADA activity and serum ADA2 activity was increased in hyperemesis gravidarum and pre-eclampsia in pregnant women. Less information is available regarding role of ADA in abortions (recurrent and missed) and anembryonic pregnancies. Here, we review the activity of ADA and its isoenzymes. Despite these findings, it will be interesting to know whether activity of ADA will be same if ADA is estimated throughout the pregnancy and in pregnancy related complications from early first trimester to third trimester, as all studies until now were carried out at a particular stage of pregnancy.

Adenosine, an endogenous anti-inflammatory metabolite, is increased in response to inflammation produced by adipose tissue in obesity. However, adenosine deaminase acts on adenosine to convert it into inosine, thereby increasing adenosine deaminase activity in overweight and obese Indian subjects.

SummaryThe aim of present study was to assess the association between serum zinc and oxidant/antioxidant status in children with protein energy malnutrition. Serum zinc, total antioxidant capacity and malondialdehyde were measured spectrophotometrically in 100 children (6 mo to 5 y); out of these, 50 children were malnourished and 50 children served as controls. Serum zinc levels were found to be significantly low in the malnourished ( p Ͻ 0.001). Serum zinc levels in Grade I and Grade II malnourished were 82.7 and 67.7 g/ dL respectively and in Grade III and IV combined was 53.2 g/dL as compared to 109.5 g/ dL in the control group. These levels were significantly lower in children who had skin lesions than in those without such lesions ( p Ͻ 0.001). Total antioxidant capacity was found to be significantly lowered in malnourished children (Grade I ϭ 1.3 mmol/L, Grade II ϭ 1.1 mmol/L, Grade III and IV ϭ 0.5 mmol/L) as compared to 2.0 mmol/L in the control group ( p Ͻ 0.001). The malondialdehyde concentration in malnourished children was significantly higher ( p Ͻ 0.001) (Grade I ϭ 1.6 nmol/mL, Grade II ϭ 1.9 nmol/mL, Grade III and IV ϭ 2.9 nmol/mL) as compared to 1.3 nmol/mL in controls. Total antioxidant capacity and hypoalbuminaemia were also correlated positively with low serum zinc level. Serum trace element deficiency leading to depleted antioxidant protection may be a contributing factor to the pathophysiology of protein energy malnutrition and replacement of these elements in the management of this condition might be important.

The significant increase in serum MDA concentration associated with the decrease in serum TAC, Zn and ALP in malnourished children suggest that these children were potentially susceptible to high oxidative stress. Current study also suggest that conventional measures of detecting under-nutrition (low weight-for-age) may be missing out a considerable proportion of undernourished children present in the population.

The mean ADA and ALP activity was significantly increased in pulmonary tuberculosis as compared to lung cancer subjects and hence may be a useful tool for the diagnosis of pulmonary tuberculosis.