Abstract
Background: Besides acute lethal cyanide poisoning, its chronic intoxication may also produce some pathologic effects on different tissues that precedes alterations in biochemical parameters. The present study was aimed to evaluate the effects of sublethal cyanide exposure on some tissue enzyme activities in liver and kidney of rats. Methods: Twelve male rats were divided into two groups as follows: Group 1 rats served as control. Rats in group 2 received water containing 200 ppm inorganic cyanide. At the end of the experiment (42 days), hepatic and renal activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and rhodanese were measured. Results: Potassium cyanide administration caused elevation of all measured liver enzymes in group 2, although the increase was only significant for AST and ALT activities as compared to control values (P<0.05). Moreover, renal AST activity in rats from group 2 was significantly higher than those from controls. Conclusion: The altered tissue activities of some enzymes in the present study might reflect the metabolic disturbances due to cyanide intoxication in studied organs. However, further research should be focused on this issue for better understanding of the fine mechanism of cyanide effects upon metabolic enzyme activities.
Highlights
Cyanide (CN-) is a potent inhibitor of aerobic metabolism, acting on cytochrome oxidase, the final component of the mitochondrial respiratory chain
Besides acute lethal cyanide poisoning, its chronic intoxication may produce some pathologic effects on different tissues that precedes alterations in biochemical parameters
The present study was aimed to assess the effects of sub-lethal cyanide exposure on tissue enzyme alterations of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and rhodanese in liver and kidney of rats
Summary
Cyanide (CN-) is a potent inhibitor of aerobic metabolism, acting on cytochrome oxidase, the final component of the mitochondrial respiratory chain. Deaths from acute cyanide intoxication have been documented in several species of animals [3, 4]. Besides acute lethal cyanide poisoning, its chronic intoxication may produce some pathologic effects on different tissues that precedes alterations in biochemical parameters. Chronic cyanide intoxication has induced alterations in some tissue biochemical, histological and oxidative stress parameters in experimental animal models [2, 7,8,9,10,11,12]. Species differences have been reported on the organ-specific biochemical markers and the susceptibility to various toxic agents [13]. The present study was aimed to assess the effects of sub-lethal cyanide exposure on tissue enzyme alterations of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and rhodanese in liver and kidney of rats
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