Study of Acetyl Cholinesterase, Butyryl Cholinestrase and β - Glucuronidase in Organophosphorus Poisoning.

Organophosphorus poisoning is common problem throughout the world. It occurs due to accidental exposure; suicidal and homicidal attempt. Many deaths occur within hours of ingestion of organophosphorus compounds like pesticides. For its prevention, speedy diagnosis and prompt treatment is required; which requires sensitive marker/s. The aim of this study was to find such marker/s. In this regard, activities of Acetylcholinesterase, Butyrylcholinesterase and β-glucuronidase were estimated in 80 samples including 40 controls and 40 organophosphorus poisoning cases (mild = 07, moderate = 19 and severe = 14). Results indicated that activities of Acetylcholinesterase and Butyrylcholinestrase decrease in mild, moderate and severe Organophosphorus poisoning in proportionate manner whereas, β-glucuronidase activity increases as severity of Organophosphorus poisoning progresses. Thus, all the three enzymes showed alterations in their activities however, the degree of change in activity was maximum in case of Acetylcholinesterase. Thus, Acetylcholinesterase activity is the most sensitive marker amongst three enzymes in Organophosphorus poisoning.

Level of nitric oxide and antioxidant vitamins in sickle cell anaemia patients.

Sickle cell anaemia (SCA) is characterized with sever anaemia and vasoocclussive episodes. Nitric Oxide (NO) a potential vasodilator, synthesized from various cells including endothelial cell. However SCA is associated with endothelial dysfunction, a measure cognitive factor for pulmonary hypertension (PH) and vasoocclussive crisis. The present study was attempted to evaluate level of serum NO and plasma antioxidant vitamins A, E and C in homozygous (n=30) and heterozygous (n=30) sickle cell patients and compared with age and sex matched healthy controls (n=30). We found, significantly (P<0.0001) elevated level of serum NO and significantly (P<0.0001) depleted antioxidant vitamins in homozygous and heterozygous sickle cell patients compared to healthy controls. Our study reveals that oxidative stress may be a responsible factor for the reduced bioavailability of NO which can impair the vasodilation in sickle cell patients.