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.

Gibberellic acid (GA3) is a well-known plant growth regulator used in several countries, but its widespread use has negative effects on both animal and human health. The current study assesses the protective effect of royal jelly (RJ) and Chlorella vulgaris (CV) on the genotoxicity and hepatic injury induced by GA3 in rats. Daily oral administration of 55 mg/kg GA3 to rats for 6 constitutive weeks induced biochemical and histopathological changes in the liver via oxidative stress and inflammation. Co-administration of 300 mg/kg RJ or 500 mg/kg CV with GA3 considerably ameliorated the serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), ALP (alkaline phosphatase), γGT (gamma-glutamyl transferase), total bilirubin, and albumin. Lowered malondialdehyde, tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB) levels along with elevated SOD (superoxide dismutase), CAT (catalase), and GPx (glutathione peroxidase) enzyme activities indicated the antioxidant and anti-inflammatory properties of both RJ and CV. Also, they improved the histological structure and reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions along with up-regulating peroxisome proliferator activated receptor α (PPARα) and down-regulating activator protein 1 (AP-1) gene expression. Additionally, chromosomal abnormalities and mitotic index were nearly normalized after treatment with RJ and CV. In conclusion, RJ and CV can protect against GA3-induced genotoxicity and liver toxicity by diminishing oxidative stress and inflammation, and modulating the PPARα/AP-1 signaling pathway.

Sesame oil has been exhibited to have anti-in ammatory and antioxidant in uences. The goal of this experiment was to look into sesame oil's hepato-protective properties and underlying processes in valproic acid-induced hepatotoxicity. Molecular docking was carried out to clarify the functional and structural underlying mechanism of sesame oil ameliorative effect. Mice were given 8 ml/kg/day of sesame oil (orally) and 100 mg/kg/day of valproic acid (i.p.) for 21 days. The results revealed that valproic acid caused a considerable increase in hepatic malondialdehyde (MDA) levels while decreasing the activity of glutathione peroxidase (GPx) enzyme. There was also a signi cant rise in serum levels of interleukines 1β & 6 (IL-1β & IL-6) and a signi cant decrease in hepatic (PXR) gene expression level.Sesame oil co-administration with valproic acid signi cantly normalized the antioxidant and antiin ammatory status and upregulated the gene expression level of PXR. In silico docking analysis results con rmed these results. This study concluded that supplementation of sesame oil attenuated valproic acid induced oxidative stress and in ammation. Hence, it was recommended as a dietary supplement for protection against valproic acid induced hepatotoxicity.

Background Cisplatin is a wide-ranging antineoplastic drug. Neurotoxicity is one of cisplatin’s side effects that restrict its usage. This study aimed to investigate the possible protective properties of sweet basil oil against cisplatin-induced neurotoxicity in mice. A docking study was carried out to elucidate the fundamental mechanism of sweet basil oil’s ameliorative influence. Thirty male mice were allocated into three groups as follows: control group, cisplatin group (2.3 mg/kg), and sweet basil oil group (25 µl/kg basil oil + cisplatin 2.3 mg/kg). Cisplatin was given for five successive days, followed by five days of rest, for two cycles, while sweet basil oil was orally administered for 21 successive days. Results Our results revealed that sweet basil oil’s antioxidant activity ameliorated the oxidative stress induced by cisplatin in mice’s brains via lowering MDA levels and increasing CAT activity and Nrf2 levels. Also, the anti-apoptotic activity of sweet basil oil was obvious via lowering the gene expression levels of Bid and caspase-3 but did not affect the serum level of P38 MAPK. Changes in acetylcholinesterase activity, serotonin and dopamine levels induced by cisplatin were significantly alleviated by sweet basil oil. Conclusion Sweet basil oil can be used as a food supplement to guard against cisplatin-induced neurotoxicity. Graphical abstract

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