Modulatory effect of thymol on the immune response and susceptibility to Aeromonas hydrophila infection in Nile tilapia fish exposed to zinc oxide nanoparticles.

Zinc oxide nanoparticles (ZnO-NPs) have many exciting properties that make their use in a continuous increase in various biomedical, industrial, and agricultural applications. This is associated with accumulation in the aquatic ecosystems and fish exposure with consequent deleterious effects. To determine the potential of thymol to counteract the immunotoxic effects of ZnO-NPs, Oreochromis niloticus was exposed to ZnO-NPs (⅕ LC50 =1.14 mg/L, for 28 days) with or without feeding a thymol-incorporated diet (1 or 2 g/kg diet). Our data demonstrated a reduction of aquaria water quality, leukopenia, and lymphopenia with a decrease in serum total protein, albumin, and globulin levels in exposed fish. At the same time, the stress indices (cortisol and glucose) were elevated in response to ZnO-NPs exposure. The exposed fish also revealed a decline in serum immunoglobulins, nitric oxide, and the activities of lysozyme and myeloperoxidase, in addition to reduced resistance to the Aeromonas hydrophila challenge. The RT-PCR analysis showed downregulation of antioxidant (SOD) superoxide dismutase and (CAT) catalase gene expression in the liver tissue with overexpression of the immune-related genes (TNF-α and IL-1ß). Importantly, we found that thymol markedly protected against ZnO-NPs-induced immunotoxicity in fish co-supplemented with thymol (1 or 2 g/kg diet) in a dose-dependent manner. Our data confirm the immunoprotective and antibacterial effects of thymol in ZnO-NPs exposed fish, supporting the potential utility of thymol as a possible immunostimulant agent.

Sesamol protects against aluminum oxide nanoparticles-induced hepatorenal toxicity in rats via modulation of oxidative stress, inflammation, apoptosis, and DNA damage.

Aluminum oxide nanoparticles (Al2 O3 -NPs) are exceedingly used in various industrial and commercial applications, providing growing concerns about their potential adverse impacts on animals and human health. Therefore, the present study was conducted to evaluate the potential protective effect of sesamol (SML) against the induced hepatorenal toxicity of Al2 O3 -NPs. Forty male rats were randomly assigned into four groups and treated orally for 28 consecutive days. Control group received distilled water. SML group received SML (100 mg/kg bw). Al2 O3 -NPs group received Al2 O3 -NPs (100 mg/kg bw). SML + Al2 O3 -NPs group received SML 2 h prior to Al2 O3 -NPs. The results revealed that Al2 O3 -NPs significantly increased serum alanine aminotransferase and aspartate aminotransferase activities and serum urea and creatinine levels. Moreover, Al2 O3 -NPs induced a significant elevation in malondialdehyde level with significant reduction in reduced glutathione content and catalase and superoxide dismutase activities, together with a marked increase of 8-hydroxy-2-desoxyguanosine level in the hepatic and renal tissues. Also, up-regulations of glutathione-S-transferase, tumor necrosis factor-alpha, and caspase-3 mRNA gene expressions were recorded in the liver and kidneys. Additionally, Al2 O3 -NPs induced multifocal areas of necrosis in hepatic parenchyma with glomerular mesangial cell proliferation and glomerular sclerosis in kidney tissues. Conversely, concomitant treatment with sesamol mitigated Al2 O3 -induced hepatorenal toxicity evidenced by improvement of liver and kidney functions that correlated with regulation of oxidant/antioxidant status, inflammatory, and apoptotic biomarkers and reduction of DNA and tissues damages. In conclusion, sesamol could exert a promising protective role against hepatorenal toxicity of Al2 O3 -NPs, possibly via its antioxidant, anti-inflammatory and anti-apoptotic properties.

Neuroprotective effect of sesamol against aluminum nanoparticle-induced toxicity in rats.

Alumina nanoparticles (ALNPs) are widely used causing neurobehavioral impairment in intoxicated animals and humans. Sesamol (SML) emerged as a natural phytochemical with potent antioxidant and anti-inflammatory properties. However, no study has directly tested the potential of SML to protect against AlNP-induced detrimental effects on the brain. AlNPs (100 mg/kg) were orally administered to rats by gavage with or without oral sesamol (100 mg/kg) for 28 days. In AlNP-intoxicated group, the brain AChE activity was elevated. The concentrations of MDA and 8-OHdG were increased suggesting lipid peroxidation and oxidative DNA damage. GSH depletion with inhibited activities of CAT and SOD were demonstrated. Serum levels of IL-1ß and IL-6 were elevated. The expressions of GST, TNF-α, and caspase-3 genes in the brain were upregulated. Histopathologically, AlNPs induced hemorrhages, edema, neuronal necrosis, and/or apoptosis in medulla oblongata. The cerebellum showed loss of Purkinje cells, and the cerebrum showed perivascular edema, neuronal degeneration, necrosis, and neuronal apoptosis. However, concomitant administration of SML with AlNPs significantly ameliorated the toxic effects on the brain, reflecting antioxidant, anti-inflammatory, and anti-apoptotic effects of SML. Considering these results, sesamol could be a promising phytochemical with neuroprotective activity against AlNP-induced neurotoxicity.