Zinc Oxide Nanoparticles Ameliorate Aluminum Chloride-Induced Hepato-Renal Oxidative Stress and Inflammation in Rats

Mahmoud, Sahar M.; Kassab, Rami B.; Moneim, Ahmed E. Abdel

doi:10.22159/ijpps.2020v12i1.35956

Cited by 2 publications

(2 citation statements)

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“…The present results indicated that co-treatment of ATZ group with ZnO-NPs could decrease mRNA expression levels of NF-κB and TNF-α, which could be attributed to the anti-inflammatory activity of ZnO-NPs. These findings come in agreement with Mahmoud et al [ 54 ]. Moreover, Kim and Jeong [ 55 ] revealed that ZnO-NP exposure inhibited the nuclear translocation of NF-κB by blocking IκBα phosphorylation and degradation and consequently decreasing the production of IL-1β and TNF-α in LPS-induced RAW macrophages.…”

Section: Discussionsupporting

confidence: 94%

“…The co-treatments of ATZ-exposed rats with zinc oxide nanoparticles or ascorbic acid in our study modulated the alteration in ALT and AST enzymes and come in line with Mahmoud et al [ 54 ] and Hamza et al [ 83 ], respectively, which also restored the normal levels of total proteins and albumin as in agreement with Hassan et al [ 84 ] and Abou-Kassem et al [ 85 ], respectively, indicating their cytoprotective and antioxidant qualities. Previous studies have shown that vitamin C ameliorated the elevated serum ALT and AST activities in rat models of malathion hepatotoxicity [ 86 ] and organophosphate pesticide toxicity [ 87 ].…”

Section: Discussionsupporting

confidence: 91%

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Zinc Oxide Nanoparticles and Vitamin C Ameliorate Atrazine-Induced Hepatic Apoptosis in Rat via CYP450s/ROS Pathway and Immunomodulation

Mohammed

Safwat

Bahnasawy

et al. 2023

Biol Trace Elem Res

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Atrazine, as an herbicide, is used widely worldwide. Because of its prolonged persistence in the environment and accumulation in the body, atrazine exposure is a potential threat to human health. The present study evaluated the possible protective effects of zinc oxide nanoparticles and vitamin C against atrazine-induced hepatotoxicity in rats. Atrazine administered to rats orally at a dose of 300 mg/kg for 21 days caused liver oxidative stress as it increased malondialdehyde (MDA) formation and decreased reduced glutathione (GSH) contents. Atrazine induced inflammation accompanied by apoptosis via upregulation of hepatic gene expression levels of NF-κB, TNF-α, BAX, and caspase-3 and downregulation of Bcl-2 gene expression levels. Additionally, it disturbed the metabolic activities of cytochrome P450 as it downregulated hepatic gene expression levels of CYP1A1, CYP1B1, CYP2E1. The liver function biomarkers were greatly affected upon atrazine administration, and the serum levels of AST and ALT were significantly increased, while BWG%, albumin, globulins, and total proteins levels were markedly decreased. As a result of the above-mentioned influences of atrazine, histopathological changes in liver tissue were recorded in our findings. The administration of zinc oxide nanoparticles or vitamin C orally at a dose of 10 mg/kg and 200 mg/kg, respectively, for 30 days prior and along with atrazine, could significantly ameliorate the oxidative stress, inflammation, and apoptosis induced by atrazine and regulated the hepatic cytochrome P450 activities. Furthermore, they improved liver function biomarkers and histopathology. In conclusion, our results revealed that zinc oxide nanoparticles and vitamin C supplementations could effectively protect against atrazine-induced hepatotoxicity.

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Section: Discussionsupporting

confidence: 94%