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Background Acrylamide (ACR) is a well-proven neurotoxin and potential food carcinogen in humans and rodent models. Silymarin (SIL) is a flavonoid mixture isolated from seeds, leaves, and fruits of Silymarin marianum (milk thistle) that possesses a free-radical scavenging effect. Objective In this work, the primary focus was to investigate the efficacy of SIL to mitigate ACR-induced subacute neurotoxic effects and oxidative changes in rat cerebellum. Methods Adult male rats were treated intraperitoneally with ACR (50 mg/kg) with or without SIL (160 mg/kg). The neuropathology and biochemical parameters viz. lipid peroxidation (measured as levels of malondialdehyde or MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), serotonin (5-hydroxytryptamine; 5-HT), dopamine (DA), and cathepsin D (CTSD) in the cerebellum have been evaluated. Results The data showed that ACR induced redox disruptions as measured by increased MDA levels and inhibition of CAT, SOD, and GPx antioxidant enzyme activities. Besides, cerebellar monoamine neurotransmitters, 5-HT and DA, were depleted in ACR-treated rats. Furthermore, ACR administration caused a significant elevation of CTSD activity, indicating that ACR could trigger apoptosis or apoptosis-like death. At the tissue level, cerebellar cortex sections from ACR-treated animals were characterized by severe neuronal damage. The administration of SIL to ACR-treated rats remarkably alleviated all the aforementioned ACR-induced effects. Conclusion SIL has a potent therapeutic effect against ACR-induced cerebellar neurotoxicity in experimental rats via the attenuation of oxidative/antioxidative responses and the inhibition of CTSD-activity.

a-cypermethrin is one of the most potent insecticides used worldwide. This study was planned to evaluate the possible role of a-lipoic acid in a-cypermethrin induced toxicity in rats. The treated groups were; the control, α-cypermethrin, a-lipoic acid and a-cypermethrin, and a-lipoic acid groups. Our results showed that administration of a-cypermethrin caused a significant decrease in RBC count, PCV, and Hb content and an increase in WBC count. Also, a- cypermethrin caused a significant increase in the levels of cholesterol, TGs, LDL-Cand VLDL-C, while the HDL-C was decreased. Also, a-cypermethrin caused a reduction in serum testosterone, FSH, and LH levels in intoxicated rats. Furthermore, the co-administration of a-lipoic acid mitigated the toxicity of a-cypermethrin by partially normalizing these biochemical parameters. Our results were supported by histopathological observations of the testis. Our data suggest that a-lipoic acid may have a protective role against a-cypermethrin induced toxicity in rats.

Lead is one of the oldest environmental and occupational toxins. Health hazards from increased lead exposure as a result of industrial and environmental pollution are recognized. The aim of the present study was to investigate the protective effects of quercetin as a model of an antioxidant drug against the toxic effects of lead acetate on the blood and the testis of rats. The lead concentrations were determined in blood and the testis. Testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were assessed in serum. Hemoglobin (Hb) content, packed cell volume (PCV), white blood cell (WBC) and red blood cell (RBC) counts were evaluated in the whole blood. Our results showed that administration of lead acetate was associated with an increased lead levels in blood as well as in the testis. Lead acetate administration also caused a decrease in testicular function, Hb content, PCV and RBC count in comparison to the respective mean values of the control. In addition, lead acetate increased WBC count and induced alterations in sperm count, sperm motility and sperm abnormality and histopathology. In the contrary, administration of lead acetate along with quercetin partially restored the studied parameters to normal values. In conclusion, the treatment with quercetin may provide a partial protection against the toxic effects induced by lead acetate in blood and the testis of rats.

The present work aims to evaluatethe cytotoxic effects on lung cells exerted by gasoline. 60 male albino mice were used in the present experiment, divided equally into 3 groups: first group (control) was left access to fresh air, second group (experimental) was subjected to gasoline 80- vapor/1h./day and third group (experimental) was subjected to gasoline 90-vapor/1h./day along eight consecutive weeks. The study comprises determination of body weight, bioaccumulation of some heavy metals ,histological and ultra-changes . Histological changes increased according to duration of exposure as, infiltration of inflammatory cells, detachment and necrosis of the epithelial cells .The electron micrographs revealed dilatation of the smooth endoplasmic reticulum, loss of the secretory granules in the Clara cells and loss of cilia in the ciliated cells that exhibited bleb formation. Necrotic type II pneumocytes, exhibited vacuolation, fragmentation of the rough endoplasmic reticulum,mitochondrial degeneration , nuclear alterations, degeneration of lamellar bodies and microvillar atrophy. In conclusion, gasoline vapour inhalation induced lung tissue injury and cellular damage concomitant with impairment of the lung antioxidant defense system. These effects were more pronounced with the unleaded than with the leaded gasoline.

Rutin, a food derived-polyphenolic bioflavonoid, has been acknowledged for several health benefits. This study aims to explore the ameliorative effects of rutin against carbon tetrachloride (CCl4) toxicity in male rats. Adult male rats were given either CCl4 (30% in olive oil, 3 ml/kg b.w. intraperitoneally) alone or in combination with rutin (70 mg/kg intragastrically) twice a week for 4 weeks. Our data showed that rutin mitigated CCl4 hepatorenal damage, as indicated by diagnostic markers (i.e., transaminases, alkaline phosphatase, total bilirubin, total protein, albumin, urea, uric acid and creatinine), and histopathological findings. In addition, CCl4 induced profound elevation of free radical generation and oxidative stress, as evidenced by increasing lipid peroxidation and reducing catalase, superoxide dismutase and glutathione peroxidase activities in liver, kidney and testicular tissues; these effects were suppressed by coexposure with rutin. Moreover, the increase in the levels of serum triglycerides, cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol induced by CCl4 was effectively counteracted by rutin. The decrease in the level of high-density lipoprotein cholesterol in the CCl4 group was also counteracted by rutin treatment. Interestingly, the decreased levels of hormonal mediators associated with sperm production, including serum testosterone, luteinizing hormone and follicle-stimulating hormone, and the impaired sperm quality induced by CCl4 were reversed by rutin. Data from the current study clearly demonstrated that rutin supplementation could at least partly overcome CCl4-induced hepatotoxicity, nephrotoxicity and reproductive toxicity by antioxidant and antidyslipidemic effects.