Superoxide Dismutase (Sod) Activity And Serum Calcium Level In Rats Exposed To A Locally Produced Insecticide “Rambo Insect Powder”

Abstract

Studies of superoxide d smutase (SOD) induction in rats exposed to locally produced insecticide; " Rambo " of which the active chemical compound is permethrin (0.6% w/w) was performed. The calcium levels in the blood p asma of the exposed rats were also evaluated. The rats were div ded into three groups of f ve rats per cage Each group of rats was fed with 1 %, 5 % or 10 % of the insecticide in their d ets The control group was fed normal d et. The effect of insecticide at various concentrations on superoxide d smutase (SOD) activ ty in the blood plasma was not s gnificantly different (P > 0.05) in the newly weaned rats (NWR). However, in the middle-aged rats (MAR) and aged rats (AR) groups, the results were s gni icantly d f erent (P < 0.05) against the parallel controls. Comparison of the ef ect of the insecticide on SOD induction at various concentrations among the groups based on age difference showed significantly dif erent result (P < 0 05), especially among the groups fed with 10 % (w/w) of the insecticide in the diet. Serum Ca 2+ level (0.51 ± 0.22mg/ml) increased rom newly weaned rats groups to (0.66 ± 0.24mg/ml) in the middle-aged rats and (0.63 ± 0.04mg/ml) for the aged rats The observed Ca 2+ increase was significantly high for rats fed 10 % (w/w) concentration of the insecticide in the diet (P < 0.05). This increase tends to suggest a concentration-dependent effect. The no-observed-effect-concentration (NOEC) was ound to be 0.006 g permethrin per 100 g of the d et, which is equivalent to 1% of the " Rambo " insecticide per 100g of the feed. Results of this study show that in non-target organisms " Rambo " insect powder may induce superox de dismu ase activity, thus suggesting, oxidative-stress related toxicity. The observed increase in calcium ion especially at 10 % (w/w) of the insecticide showed that permethrin may induce toxic effects associated with cell dea h via mitochondria uncoupling and loss in ATP metabolism.