Effect of the organophosphate [curacron] on activity of acetylcholinesterase in different parts of rat brain [in vivo studies]

Curacron profenofos is 0-[4-Bromo-2 chlorophenyl]-O-ethyi-S-propyl phosphorothioate. Its chemical formula C11H15BrCIO3PS. It is a broad-spectrum organophosphorous insecticide for control of pests in cotton growing areas. Inhibition of acetyi and pseudocholinesterase by this compound results in signs and symptoms of toxicity signs and symptoms [cholinergic syndrome]: bradycardia, respiratory-circulatory arrest, vomiting and diam'iea in a variety of animals including man. In this work experiments were carried out in vivo to study its effect on the activity of AChE enzyme obtained from whole and five different parts of rat brain, namely basal ganglia, frontal cortex, medulla oblongata, pons, and cerebellum. This work was carried out by 2 experiments: Exp. A: Depending on the dose of intraperitoneal infusion of curacon. Exp. B: Depending on the time course post infusion of a constant dose of curacron 100 mg/kg BW [dose causing 50% inhibition] in vivo. The results showed that the inhibition occurred in all brain parts, but it was highly marked in the enzyme obtained from the cerebellum [the part responsible for balance and coordination of movements]. The results also indicated that the inhibition of AChE produced by i.p. injection with curacon was dose and time dependent

Dysfunctional nitric oxide and 8-epi-prostaglandin F2alpha synthesis in healthy smokers

Background: Cigarette smoking, a major cardiovascular risk factor, has been shown to be associated with impaired endothelium- dependent vasodilatation [EDV]. Nitric Oxide [NO] being a primary vasodilator produced by endothelial cells, its production is probably affected by cigarette smoking. Cigarette smoke contains superoxide anions and a great number of other reactive oxygen species [ROS], the accumulation of which brings about oxidative damage of endothelial cells. A free radical catalyzed isomers of arachidonic acid [8-epi- PGF2infinity] is a potent vasoconstrictor and serves as a marker of oxidative stress

Objective: To evaluate the level of serum [NO] and urinary 8-epi- PGF2infinity in mild, moderate, and heavy smokers and to correlate their levels with urinary cotinine which is considered a sensitive markers of exposure to nicotine of tobacco smoke

Subjects: 20 heavy smokers, 20 moderate smokers, 20 mild smokers, and 20 controls were the material of the present study

Results: The present study revealed significant increase in urinary 8-epi- PGF2infinity in smokers compared to control subjects. Also significant increase was found in urinary 8-epi- PGF2infinity in heavy compared with moderate smokers. However, there was a significant decrease in serum [NO] in the same two groups as compared to controls. Positive correlation for urinary 8-epi- PGF2infinity and negative correlation for serum [NO] as compared to urinary cotinine were detected. It may be concluded that concentration of 8-epi- PGF2infinity and cotinine in the urine as well as NO in the sera of smokers might give more accurate information about ROS which play an important role in the pathogenesis of many diseases affecting the physiological functions of body systems