Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups; the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards.

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Objective: The paper’s primary goal is to report the devastating impact of carbon tetrachloride (CCl 4 ) on rat testicular tissue and the possible protecting function of propolis against CCl 4 based on its free radical scavenging and inflammatory relief properties. Materials and Methods: A total of 24 adult male albino rats had been classified into four groups (six rats/group). Rats of group 1 served as control, whereas groups 2–4 received propolis (200 mg/kg/day), CCl 4 (3 ml/kg/day), and propolis/CCl 4 , respectively. After 4 weeks, the collected sera were applied for the estimation of lipid profile and sex hormones. Also, histopathological picture, malondialdehyde, and tumor necrosis factor alpha (TNFα) gene profile was measured in collected testicular tissues. Results: The present information revealed a noteworthy change ( p < 0.05) in lipid profile, decrease in testicular weight, testosterone, antioxidants values along with a prominent increase ( p < 0.05) in estradiol, lipid peroxidation values, and expression of TNFα in rats administrated with CCl 4 compared to control. Moreover, the histopathological profile showed the degeneration of the epithelium. Interestingly, propolis attenuated the destructive effect of CCl 4 on rat testes. Conclusion: The examined dose of propolis reduced oxidation, and inflammatory reactions resulted from CCl 4 exposure and proved that it might have a helpful part in free radicals interceded diseases.

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bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats. Vet. arhiv 90, 57-68, 2020. AbSTrACT Bisphenol, used in many polycarbonate plastics and epoxy resins industries, exerts toxic effects on mammalian organs. The mechanisms underlying bisphenol toxicity are well understood, however the chemoprevention effects of L-carnitine have not yet been recorded. This study aimed to explore the protective mechanism of L-carnitine against BPA-induced hepatotoxicity. Male rats were randomly distributed into 4 groups of 10 rats each: vehicle (5 mL corn oil/kg), bisphenol (50 mg/kg b.w. orally), L-carnitine (500 mg/kg b.w. i/p), and L-carnitine bisphenol pre-treated groups. Bisphenol was dissolved in corn oil and gavaged for 70 consecutive days. Up-regulation of tumor necrosis factor (6.6-fold), and interleukin 6 (3.2-fold) mRNA transcript, along with suppression of nuclear factor erythroid 2-like 2 (0.4-fold), were recorded, following bisphenol administration. Subsequently, bisphenol provoked oxidative stress and attenuated the antioxidative molecules. Finally, hepatic dysfunction was assessed by elevated serum aminotransferases, alkaline phosphatase, lactate dehydrogenase, glutamyl transferase activities and ammonia levels, with the subsequent decline in serum albumin concentration, which confirmed the inflammatory cell infiltration and hydropic degeneration, and the impairment of lipid profile. Interestingly, co-administration of L-carnitine improved liver function and lipid profile, which was explained by the activation of nuclear factor erythroid 2-like 2 (1.5-fold) mRNA transcript, which augmented the antioxidant levels and suppressed oxidative stress, tumor necrosis factor (2.6fold), and interleukin 6 (1.5-fold) gene expression. In conclusion, L-carnitine exerted hepatoprotective activity against bisphenol toxicity via antioxidant and anti-inflammatory effects.