Abstract:
:Paraquat (PQ) is a relatively safe and effective herbicide used all over the world. PQ is very toxic to all living organisms; and many cases of acute poisoning and death have been reported over the past decade. The main suggested potential mechanism for PQ toxicity is the production of superoxide radicals from the metabolism of the PQ by microsomal enzyme systems, and by inducing mitochondrial toxicity. Mitochondria are considered to be a major source of reactive oxygen species in cells and according to this hypothesis, PQ, through suitable oxidation and reduction processes, is able to participate in the redox system in mitochondria. The potential ability of PQ to accept electrons from complex (I, II, III, IV) leads to rapid reaction with molecular oxygen to yield superoxide anion which can lead to the formation of more toxic reactive oxygen species, e.g., hydroxyl radical, often taken as the main toxicant. Lipid peroxidation due to PQ has been implicated in a number of deleterious effects such as increased membrane rigidity, osmotic fragility, decreased mitochondrial components, reduced mitochondrial survival and lipid fluidity. The biological effect of reactive oxygen species (ROS) is controlled by a wide spectrum of enzymatic and non-enzymatic defense mechanisms such as superoxide dismutas (SOD), catalase (CAT) and glutathione. According to this hypothesis, the chemical cascades lead to the reduction of PQ, which reacts quite rapidly with molecular oxygen to yield superoxide anion. The generation of free radicals and lipid peroxidation are the main factors that lead to mitochondrial damage.
journal_name
Environ Toxicol Pharmacoljournal_title
Environmental toxicology and pharmacologyauthors
Mohammadi-Bardbori A,Ghazi-Khansari Mdoi
10.1016/j.etap.2008.02.009subject
Has Abstractpub_date
2008-07-01 00:00:00pages
1-5issue
1eissn
1382-6689issn
1872-7077pii
S1382-6689(08)00042-2journal_volume
26pub_type
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