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Abstract
Although the effects of acute pesticide poisoning are well known but, hardly any data
exists regarding the health effects after long-term low-level exposure. Major unresolved
issues include the effect of moderate exposure in the absence of poisoning. The present
study elucidates a possible mechanism by which chronic organophosphate exposure (dichlorvos
6 mg/kg b.wt., s.c. for 12 weeks) causes liver dysfunction. Mitochondria, a primary
site of cellular energy generation and oxygen consumption represent a likely target
for organophosphate poisoning. Therefore, the objective of the current study was planned
with an aim to investigate the effect of chronic dichlorvos exposure on liver mitochondrial
electron transport chain (ETC), mitochondrial calcium uptake and its implications
on the induction of liver enzymes and liver dysfunction in rodent model. Our results
indicated decreased mitochondrial electron transfer activities of cytochrome oxidase
along with altered mitochondrial complexes I and II activity. This decrease in the
activities of electron transport complexes in turn affected the ATP synthesis and
ATP levels adversely in the mitochondria isolated from dichlorvos (DDVP) treated rat
liver. Mitochondrial preparation from DDVP treated rat liver demonstrated significant
increase in mitochondrial Ca(2+) uptake and increase ROS levels. The alterations in
the mitochondrial calcium uptake, mitochondrial electron transfer enzyme activities
and increase ROS levels in turn might have caused an increase in liver enzymes (ALT,
AST and ALP). The electron micrographs of liver cells depicted morphological changes
in mitochondria as well as nucleus following 12 weeks of exposure to DDVP. These studies
provide an evidence of impaired mitochondrial bioenergetics which may lead to liver
dysfunction after chronic exposure to dichlorvos.
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