BMC pharmacology & toxicology · 2025
Co-treatment of β-carotene with acetamiprid provides protection against acetamiprid induced hepatic and renal toxicity via modulation of the antioxidant system.
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Awadalla Eatemad A, Amin Yahia A, Ali Rana A, Gbr Samia A, Gelany Wafaa Ibraheem, Nour Amna H M
Аннотация
BACKGROUND: Acetamiprid (ACMP), one of the most widely used and effective insecticides globally, can pose potential toxicity to mammals. β-carotene (βC) is a prominent carotenoid precursor to vitamin A and exhibits antioxidant properties. This study evaluated the protective effect of βC as an antioxidant against ACMP toxicity in rats.
METHODS: A total of 40 male albino rats were divided into four groups: the control group received 1% DMSO; the βC group received 100 mg/kg of β-carotene; the ACMP group received 40 mg/kg of acetamiprid; and the ACMP + βC group received both ACMP and βC. Liver and kidney tissues were used for biochemical analyses (total oxidative stress [TOS] and total antioxidant capacity [TAC]), as well as histopathological, histochemical, and immunohistochemical analyses (MPO immunostaining).
RESULTS: The ACMP group, compared to the control and βC groups, showed a significant increase in TOS levels (p < 0.001) in both liver and kidney tissue homogenates, along with a significant decrease in TAC in the same tissues. The ACMP + βC group exhibited significantly lower TOS levels (p < 0.01) and significantly higher TAC levels (p < 0.05) than the ACMP group in the liver and kidney tissue homogenates. Furthermore, histopathological alterations were observed in both organs. Changes such as congestion of central veins and blood sinusoids in the liver were noted. In most cases, hepatocytes exhibited basophilic cytoplasm, vacuolar cytoplasm, and pyknotic nuclei. Renal alterations included atrophy of the renal corpuscle, reduced glomerular cellularity, marked dilation of the urinary space, desquamated epithelial cells in the tubular lumen, inflammatory cell infiltration, and congestion of interstitial blood capillaries. In contrast, the ACMP + βC group showed significant improvements in these histopathological changes. MPO immunostaining revealed a significant increase in the ACMP group compared to the other three groups.
CONCLUSION: Co-treatment with β-carotene and acetamiprid reduced ACMP-induced toxicity by enhancing antioxidant capacity and reducing oxidative stress.
METHODS: A total of 40 male albino rats were divided into four groups: the control group received 1% DMSO; the βC group received 100 mg/kg of β-carotene; the ACMP group received 40 mg/kg of acetamiprid; and the ACMP + βC group received both ACMP and βC. Liver and kidney tissues were used for biochemical analyses (total oxidative stress [TOS] and total antioxidant capacity [TAC]), as well as histopathological, histochemical, and immunohistochemical analyses (MPO immunostaining).
RESULTS: The ACMP group, compared to the control and βC groups, showed a significant increase in TOS levels (p < 0.001) in both liver and kidney tissue homogenates, along with a significant decrease in TAC in the same tissues. The ACMP + βC group exhibited significantly lower TOS levels (p < 0.01) and significantly higher TAC levels (p < 0.05) than the ACMP group in the liver and kidney tissue homogenates. Furthermore, histopathological alterations were observed in both organs. Changes such as congestion of central veins and blood sinusoids in the liver were noted. In most cases, hepatocytes exhibited basophilic cytoplasm, vacuolar cytoplasm, and pyknotic nuclei. Renal alterations included atrophy of the renal corpuscle, reduced glomerular cellularity, marked dilation of the urinary space, desquamated epithelial cells in the tubular lumen, inflammatory cell infiltration, and congestion of interstitial blood capillaries. In contrast, the ACMP + βC group showed significant improvements in these histopathological changes. MPO immunostaining revealed a significant increase in the ACMP group compared to the other three groups.
CONCLUSION: Co-treatment with β-carotene and acetamiprid reduced ACMP-induced toxicity by enhancing antioxidant capacity and reducing oxidative stress.