Thiacloprid (TH) is a neurotoxic agricultural insecticide and potential food contaminant. The purpose of this study was to investigate the relationship between TH exposure and memory dysfunction in rats, as well as the potential protective effect of piracetam and piracetam-loaded magnetic chitosan nanoparticles (PMC NPs). Rats were divided into five equal groups (six rats/group). The control group received saline. Group II was treated with PMC NPs at a dose level of 200 mg/kg body weight (Bwt); Group III was treated with 1/10 LD50 of TH (65 mg/kg Bwt); Group IV was treated with TH (65 mg/kg Bwt) and piracetam (200 mg/kg Bwt); Group V was co-treated with TH (65 mg/kg Bwt) and PMC NPs (200 mg/kg Bwt). All animal groups were dosed daily for 6 weeks by oral gavage. Footprint analysis, hanging wire test, open field test, and Y-maze test were employed to assess behavioral deficits. Animals were euthanized, and brain tissues were analyzed for oxidative stress biomarkers, proinflammatory cytokines, and gene expression levels of glial fibrillary acidic protein (GFAP), amyloid-beta precursor protein (APP), B-cell lymphoma 2 (Bcl-2), and caspase-3. Brain and sciatic nerve tissues were used for the evaluation of histopathological changes and immunohistochemical expression of tau protein and nuclear factor kappa B (NF-κB), respectively. The results revealed that TH-treated rats suffered from oxidative damage and inflammatory effect on the central and peripheral nerves. The administration of PMC NPs considerably protected against TH-induced neuronal damage, increased antioxidant enzyme activity, decreased inflammatory markers, and improved behavioral performance than the group treated with piracetam. The neuroprotective effect of PMC NPs was mediated through the inhibition of GFAP, APP, caspase-3, Tau, and NF-κB gene expression with induction of Bcl-2 expression. In conclusion, TH could induce oxidative stress, inflammatory and neurobehavior impairment in rats. However, PMC NPs administration markedly mitigated TH-induced brain toxicity, possibly via oxidative and inflammatory modulation rather than using piracetam alone.

Alternaria toxins are emerging mycotoxins that gained considerable interest with increasing evidence of their existence and toxicological properties. There is limited research and insufficient data about their in vivo hazardous effects. We designed this study to evaluate histopathological and genotoxic in vivo impacts of alternariol (AOH) on the parotid gland as well as to assess the competency of gallic acid (GA) in reversing these effects. Forty healthy adult male Wister rats were utilized and assigned equally on control, GA, alternariol and AOH+ gallic treated groups. Parotid gland samples from experimental groups were collected and then examined for histopathological, ultrastructural and immunohistochemical examination for 4-hydroxynonenal “4-HNE as lipid peroxidation marker” as well as Comet assay for DNA damage. Additionally, parotid tissue homogenates were tested for catalase “CAT”, superoxide dismutase “SOD” and malondialdehyde “MDA” levels. Our data proved that alternariol produced various histopathological and ultrastructural alterations of parotid acini as well as significant DNA damage, significant reduction of CAT and SOD enzymatic activity and significant boosting of 4-HNE immunohistochemical expression and MDA levels as compared to control group. On the other hand, gallic acid administration almost restored histological and ultrastructural parotid architecture, 4-HNE immune-expression and biochemical levels. Ultimately, we demonstrated alternariol-induced histopathological and genotoxic alterations on parotid gland as well as the competency of gallic acid in reversing these effects.

Objective: This experimental study aimed to evaluate the statin-induced hepatotoxicity in albino rats, as well as to compare the potential hepatotoxicity between atorvastatin and simavastatin through evaluation of both biochemical and histopathological parameters. Materials & Methods: 60 male albino rats were used in this study and were equally divided into three groups. The control group received only saline orally, the atorvastatin group which received (80 mg/kg) orally, and the simavastatin group which received simavastatin (80 mg/kg) orally. The study was conducted over a period of 12 weeks and at the end blood samples and liver tissues were obtained for assessment of biochemical markers of the liver and histopathological examination. Results: All the biochemical parameters in the current study showed higher values in the atorvastatin and simvastatin groups compared to the control group with significant probability value. The significance was detected between each of the statin groups and the control group. However no significant difference was found between atorvastatin and simvastatin group. Likewise, histopathological results showed significant hepatic injury in case of both statin groups compared to the control one. Conclusion & Recommendations: Atorvastatin and simvastatin induced hepatic injury as demonstrated by both biochemical and histopathological results in this study. Moreover, no significant difference was found between atorvastatin and simvastatin as regard statin induced liver injury.

Background: Methotrexate (MTX) is widely used as a cytotoxic chemotherapeutic agent for malignancies as well as in the treatment of various inflammatory diseases. MTX treatment has been associated with hepatic toxicity and genotoxicity. The current study was conducted to assess the potential protective role of N-acetylcysteine in attenuation of methotrexate-induced hepatic damage and genotoxicity in MTX intoxicated male albino rats.Methods: Forty, apparently healthy adult male albino rats weighed 150+10 gm were randomly divided into four groups; [group 1: negative control group, group 2: positive control (NAC treated) group, group 3: MTX treated group, group 4: MTX/NAC treated group]. The rats were treated once daily for 12 weeks by I.V injection of Methotrexate in a dose of 2 mg/kg ( 1 / 7 LD 50 ) and N-acetylcysteine in a dose of 80 mg/kg ( 1 / 14 LD 50 ) in the tail veins of rats. Blood samples were obtained at the end of the 4 th , 8 th and 12 th weeks and were prepared for ALT levels and BAX gene expression value examination. At the end of the study, liver samples were obtained for histopathological examination.Results: A significant constant increase in ALT levels and BAX gene expression value of the MTX-treated group (group 3) was observed throughout the study. Supplementation of NAC concomitantly with MTX in group 4 reduced significantly ALT levels and BAX gene expression value when compared to the non-supplemented group 3 that treated with MTX at the 4 th , 8 th and 12 th weeks (P< 0.000).The previous chemical results were confirmed by the histopathological studies of the liver that revealed the presence of dilatation and congestion of the central veins, hepatic sinusoids, hepatic arteries, portal veins with increased number of Kupffer cells and pyknosis of the hepatic nuclei in group 3: MTX treated group. On the other hand, the liver sections showed the normal hepatic architectures with addition of NAC with MTX in group 4.Conclusion: The present study showed that NAC has a good protective effect against the hepatic damage and genotoxicity induced by MTX in male albino rats.

Background: Methotrexate (MTX) is widely used as a cytotoxic chemotherapeutic agent for malignancies as well as in the treatment of various inflammatory diseases. MTX treatment has been associated with renal toxicity. The current study was conducted to assess the potential protective role of N-acetylcysteine and/or melatonin in attenuation of methotrexate-induced renal damage in MTX intoxicated male albino rats.Methods: sixty, apparently healthy adult male albino rats weighed 150+10 gm were randomly divided into six groups; (group 1: negative control group, group 2: positive control (NAC treated) group, group 3: positive control (Melatonin treated) group, group 4: MTX treated group, group 5: MTX/NAC treated group, group 6: MTX/Melatonin treated group). The rats were treated once daily for 12 weeks by I.V injection of Methotrexate in a dose of 2 mg/kg ( 1 / 7 LD 50 ), N-acetylcysteine in a dose of 80 mg/kg ( 1 / 14 LD 50 ) and Melatonin: in a daily dose of 10 mg/kg ( 1 / 36 LD 50 ) in the tail veins of rats and blood samples were obtained at the end of the 4 th , 8 th and 12 th weeks and were prepared for Creatinine examination. At the end of the study, kidney samples were obtained for histopathological examination.Results: A significant constant increase in the creatinine of the MTX-treated group (group 4) was observed throughout the study. Supplementation of NAC concomitantly with MTX in group 5 reduced significantly creatinine when compared to the non-supplemented group 4 that treated with MTX at the 4 th , 8 th and 12 th weeks. On the other hand, the use of the melatonin in combination with MTX in group 6 produced minimal non-significant reduction of the creatinine level relative to group 4 at the 4 th , 8 th and 12 th weeks (P>0.05). The previous chemical results were confirmed by the histopathological studies of the kidney that revealed maximal affection of the renal cortex in the MTX-treated rats (group 4). Kidney histopathologic findings were significantly milder when NAC was co-administered with MTX in groups 5. Meanwhile, deterioration of the renal cortical structure was observed in the MTXmelatonin treated rats (group 6).Conclusion: The present study showed that NAC has a superior protective effect than Melatonin against the renal damage induced by MTX in male albino rats.