Detection of cotinine in neonate meconium as a marker for nicotine exposure in utero

Neonate meconium cotinine level was evaluated as a marker of prenatal exposure to nicotine from tobacco smoking by mothers. Mothers admitted to a maternity hospital in Alexandria, Egypt, were divided into 3 groups: 10 active smokers, 10 passive smokers and 10 with no tobacco exposure during pregnancy. Urine and saliva samples were collected from mothers and first-day meconium samples from their neonates. Mean maternal urinary cotinine levels, measured using radioimmunoassay, differed significantly between the 3 groups, as did mean salivary cotinine and mean cotinine levels in meconium.There was a significant positive correlation between cotinine levels in meconium and both maternal urinary and salivary cotinine levels. Meconium is an ideal biological marker for testing direct fetal exposure to tobacco smoke in the neonatal period

Effect of L-arginine on the blood levels of matrix metalloproteinase-9, caspase-3 and some liver functions in cadmium chloride-induced hepatic inflammation in rats

The intent of the present work was to study the changes of some hepatic parameters upon exposure to cadmium and to study the role of L-arginine in that experimental model of hepatocellular injury. The study was conducted on thirty two adult male albino rats that were divided into four groups, a control group, a cadmium [Cd] treated group [0.1mg/kg b.w] subcutaneously for 30 days, a cadmium and saline treated group and a cadmium and L-arginine treated group [100mg/kg b.w orally] for 30 days. Cadmium significantly [P<0.05] increased the mean values of the measured parameters, alanine aminotransferase [ALT], aspartate amino transferase [AST], tumor necrosis factor alpha [TNF-a], interleukin-6 [IL-6], hepatic caspase-3 activity and serum matrix metallo-proteinase-9 [MMP-9], compared to control and to [cadmium and L-arginine]- treated rats. Concomitant administration of L-arginine with cadmium prevented the occuranee of these changes. Mean while the reduction of MMP-9 mean values, induced by L-arginine, did not return to basal control value. It was concluded that Cd-hepatocellular dysfunction, in that model, is induced through the activation of apoptosis and increased MMP-9 activity. It was also concluded that L-arginine, through the release of NO, induced a partial hepato-protective effect possibly due to the interaction of other mechanisms which may modulate MMP-9 activity