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Dichlorvos evokes systemic lipid dysmetabolism in Wistar rats: rescindment influence of curcumin


A. J. Akamo
B. A. Olagunju
O. O. Adeleye
M. A., Akinsanya
A. A., Adebisi
T. S. Adekunbi
A. F. Adenowo
F. Anifowose
O. M. Ajagun-Ogunleye
A. O. Ojelabi
O. Aluko
I. O. Opowoye
O. E. Popoola
T. E. Oladele
Y. O. Aderibigbe
C. A. Moses
S. O. Salami
O. A. Akinloye

Abstract

Organophosphorus pesticides such as dichlorvos (DDVP) are often employed to eradicate pests, especially in low and medium-income countries. However, they have several negative impacts on the visceral organs. Astonishingly, curcumin protects organs from the detrimental effects of xenobiotics via the maintenance of redox homeostasis; unfortunately, its role in dichlorvos-provoked multi-organ impairment vis-à-vis lipid homeostasis has not been examined. Therefore, this undertaking probed the remedial efficacy of curcumin on DDVP-prompted combined systemic toxicity and major lipid distribution. Randomization was engaged to dedicate rats (40) into seven groups (6 rats/group): control, DDVP only (20 mg kg-1day-1), DDVP administered with either curcumin (50 and 100 mg kg-1day-1) or reference medication atropine (0.2 mg kg-1day-1), and curcumin only (50 and 100 mg kg-1day-1). DDVP was dispensed orally for one week, followed by two weeks of curcumin treatment. Twenty-four hours after the last administration, we sacrificed the rats and collected their blood and viscera (liver, kidney, heart, lung, and brain) for bioassays. Curcumin remarkably (p<0.05) rescinded DDVP-mediated increases in plasma, LDL, and systemic cholesterol; markedly (p<0.05) attenuated DDVP-elicited decreases in HDL-cholesterol and TAG contents in all the compartments except erythrocyte and liver; and significantly (p<0.05) abated DDVP-induced plasma phospholipidaemia, multi-organ phospholipidosis, and up-regulation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA-R) activity. This finding demonstrated that curcumin reverses DDVP-triggered anomalous lipid dynamics by abating cholesterogenesis and phospholipidosis and restoring HMG-CoA-R activity.


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eISSN: 2635-3490
print ISSN: 2476-8316