engleski

Cholinesterase activity and oxidative stress in rats after paraoxon poisoning and oxime therapy

Among a large number of different types of pesticides available, organophosphates (OP) are the most frequent causes of professional, suicidal or accidental intoxications. It is generally known that OPs act as irreversible inhibitors of cholinesterases (ChE/AChE), yet there are still some open questions about their non-specific effects. Another issue concerning OP poisoning is the inability of conventional therapies to provide adequate protection. The present study was undertaken to examine the impact of possible oxidative stress on OP toxicity and the efficacy of the applied therapy. Rats were injected subcutaneously with sublethal dose of paraoxon, and treated intraperitoneally 1 min later with a combination of oxime K048 (25 % of its LD50) and atropine (10 mg kg-1). Plasma and brain samples were analysed for ChE/AChE activity and concentration of thiobarbituric reactive substances (TBARS) at four different time points (0.5 h, 1 h, 6 h and 24 h) following the treatment. It is important to stress that cholinesterase activity in both plasma and brain did not return to normal even after 24 h following the exposure to paraoxon. A combination of K048 and atropine afforded high potency in restoring the activity of ChE in plasma (50 % to 60 % up to 6 h) while an increase in AChE activity in the brain did not surpass 20 %. Although applied therapy efficiently counteracted paraoxon poisoning, determined TBARS concentrations suggested that these acute treatments resulted with free radical-mediated lipid peroxidation.

Acetycholinesterase ; Brain ; Lipid peroxidation ; Organophosphates ; Oxime K048 ; Plasma

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