Protective effects of dietary omega-3 fatty acid supplementation on organophosphate poisoning.

In this study, we aimed to study the possible preventive effect of docosahexaenoic acid (DHA), a dietary omega-3 fatty acid, on toxicity caused by chlorpyrifos (CPF). Six groups of Sprague Dawley rats (200-250 g) consisting of equal numbers of males and females (n = 8) were assigned to study. The rats were orally given for 5 days. The control group was administered pure olive oil, which was the vehicle for CPF. The CPF challenge groups were administered oral physiological saline, pure olive oil, or DHA (50, 100 and 400 mg/kg dosages) for 5 days. The animals were weighed on the sixth day and then administered CPF (279 mg/kg, subcutaneously). The rats were weighed again 24 h following CPF administration. The body temperatures and locomotor activities of the rats were also measured. Blood samples, brain and liver tissues were collected for biochemical, histopathological and immunohistochemical examinations. A comparison with the control group demonstrated that CPF administration increased malondialdehyde (MDA) levels in blood, brain and liver, while it reduced catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) concentrations ( p < 0.05-0.001). Advanced oxidation protein products (AOPPs) increased only in the brain ( p < 0.001). DHA reduced these changes in MDA and AOPP values ( p < 0.05-0.001), while it increased CAT, SOD and GPx concentrations ( p < 0.05-0.001). Similarly, DHA prevented the decreases in body weight, body temperature and locomotor activities caused by CPF at 100 mg/kg and 400 mg/kg dosages ( p < 0.05-0.001). Similar to the physiological and biochemical changes, the histopathological damage scores, which increased with CPF ( p < 0.05-0.01), decreased at all three dosages of DHA ( p < 0.05-0.01). Our findings suggest that DHA, by supporting the antioxidant mechanism, reduces toxicity caused by CPF.

Polyphenol-Rich Fraction of Parquetina nigrescens Mitigates Dichlorvos-Induced Cardiorenal Dysfunction Through Reduction in Cardiac Nitrotyrosine and Renal p38 Expressions in Wistar Rats.

Parquetina nigrescens is commonly used to treat diseases in humans and animals in developing countries, including Nigeria. This study evaluates the effects of its polyphenol-rich fraction (prf) on dichlorvos-induced cardio- and renal toxicity. There were several factors assessed during this study, including cardiac and renal markers, serum myeloperoxidase and xanthine oxidase, and electrocardiograph (ECG) changes. The changes in electrocardiograph (ECG) were recorded. Immunohistochemistry of cardiac and renal p38 and nitrotyrosine was determined. Dichlorvos exposure caused a significant decrease in L-glutathione (reduced glutathione) and other antioxidant enzymes with increases in malondialdehyde, myeloperoxidase, advanced oxidation protein products, and protein carbonyl levels. It also brought about alterations in microanatomy of the heart and kidneys accompanied by increases in serum creatinine and urea levels. Exposure to dichlorvos induced prolonged QRS interval and shortened QT durations in rats. Immunohistochemistry revealed lower expressions of cardiac nitrotyrosine and renal p38 (mitogen-activated protein kinase; MAPK) in rats treated with prf of P. nigrescens. Combining all, prf of P. nigrescens demonstrated antioxidant as well as protective properties in the heart and kidneys of rats exposed to dichlorvos. It ameliorated dichlorvos-induced cardio- and nephrotoxicity giving credence to its use in ethnomedicine.

Is intralipid fat emulsion a promising therapeutic strategy on neurotoxicity induced by malathion in rats?

AIM: Malathion is one of the most widely used organophosphate pesticides and herbicides. It has given rise to major clinical problems by its poisoning in all over the world. Malathion also a highly lipophilic agent, and tends to accumulate within lipid-rich tissue like a brain in the body, causing toxicity. Therefore, the study was aimed to investigate if there is a possible beneficial effect of using intralipid fat emulsion (IFE) on the neurotoxicity, and to detect it time-dependently at the beginning, 6th and 12th hours of M intoxication. MATERIALS AND METHODS: Forty-eight rats were randomly divided into six groups including: control (C), Lipid (L) group (18.6 mL/kg oral IFE), Malathion (M) group (10 mg/kg oral M), M0L group (IFE treated after immediate from M), M6L group (IFE treated after 6 hours from M), M12L group (IFE treated after 12 hours from M). RESULTS: M group in comparison with all others group, there was an increase in the total oxidant status (TOS) level. M group in comparison with C, L, M0L groups, it was seen significantly decrease in the total antioxidant capacity (TAC) level. Interestingly, M group in comparison with M6L and M12L groups, there was no significant difference among these groups in terms of the TAC levels. Although there was no significant difference among C, L and M0L groups in terms of both TAC and TOS levels, but was significant difference C, L groups in comparison with M6L, M12L groups in terms of TAC levels. C group in comparison with L, M0L, M6L, M12L groups in terms of TOS levels, there was no significant difference. These findings have indicated that IFE seriously reduced TOS levels in all the groups depending on time. Also, M0L group in comparison with M6L and M12L groups, there was significantly increase of the TAC levels. There was no statistically significant difference between M6L and M12L groups. These biochemical results were confirmed with immunohistochemical results. CONCLUSIONS: The study has had some certain evidence that IFE is a promising safe therapy for acutely intoxicated cases by organophosphate. It is much more effective if used at the beginning of organophosphate poisoning. As such, there is no need to avoid using IFE in clinical practice.