Abstract
Arsenic is an environmental toxicant, and one of the major mechanisms by which it exerts its toxic effect is through an impairment of cellular respiration by inhibition of various mitochondrial enzymes, and the uncoupling of oxidative phosphorylation. Most toxicity of arsenic results from its ability to interact with sulfhydryl groups of proteins and enzymes, and to substitute phosphorus in a variety of biochemical reactions. Most toxicity of arsenic results from its ability to interact with sulfhydryl groups of proteins and enzymes, and to substitute phosphorus in a variety of biochemical reactions. Recent studies have pointed out that arsenic toxicity is associated with the formation of reactive oxygen species, which may cause severe injury/damage to the nervous system. The main objective of this study was to conduct biochemical analysis to determine the effect of arsenic trioxide on the activity of acetyl cholinesterase; a critical important nervous system enzyme that hydrolyzes the neurotransmitter acetylcholine. Four groups of six male rats each weighing an average 60 +/- 2 g were used in this study. Arsenic trioxide was intraperitoneally administered to the rats at the doses of 5, 10, 15, 20mg/kg body weight (BW), one dose per 24 hour given for five days. A control group was also made of 6 animals injected with distilled water without chemical. Following anaesthesia, blood specimens were immediately collected using heparinized syringes, and acetyl cholinesterase detection and quantification were performed in serum samples by spectrophotometry. Arsenic trioxide exposure significantly decreased the activity of cholinesterase in the Sprague-Dawley rats. Acetyl cholinesterase activities of 6895 +/- 822, 5697 +/- 468, 5069 +/- 624, 4054 +/- 980, and 3158 +/- 648 U/L were recorded for 0, 5, 10, 15, and 20 mg/kg, respectively; indicating a gradual decrease in acetyl cholinesterase activity with increasing doses of arsenic. These findings indicate that acetyl cholinesterase is a candidate biomarker for arsenic-induced neurotoxicity in Sprague-Dawley rats.
Highlights
Arsenic is widely distributed in nature, being found in food, the soil, water and airborne particles; it derives from both natural and human activities [1]
The results indicate acetyl cholinesterase activities of 6895 + 822, 5697 + 468, 5069 + 624, 4054 + 980, and 3158 + 648 U/L for 0, 5, 10, 15, and 20 mg/kg body weight (BW) respectively
In order to determine the effect on serum acetyl cholinesterase (AChE), adult male SpragueDawley rats were exposed for five days to four different concentrations (5, 10, 15, 20 mg/kg) of arsenic trioxide
Summary
Arsenic is widely distributed in nature, being found in food, the soil, water and airborne particles; it derives from both natural and human activities [1]. Arsenical drugs are still used used in treating certain tropical diseases such as African sleeping sickness and amoebic dysentery, and in veterinary medicine to treat parasitic diseases, including filariasis in dogs and black head in turkeys and chickens [2]. A large number of people are exposed to arsenic chroniclly throughout the world. Humans can be exposed to arsenic through the intake of air, food and water. Food is usually the major source of arsenic exposure, most adverse effects have been associated with consumption of arsenic-contaminated drinking water. Occupational sources of arsenic to human workers include vineyards, ceramics, glassmaking, smelting and refining of metallic ores, during
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