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Aim: to investigate the sub chronic toxicity of thiamethoxam on some parameters of reproductive performance in adult male rabbits including gene expression of LDH-C4, FSHβ and LHβ and GnRHR. Method: sixteen adult male Chinchilla rabbits were divided into two equal groups. Animals in the first group were treated orally with TMX at dose of 250 mg/kg body weight for 90 days. The second group was served as control. Result: Obtained results showed that TMX increased the relative weight of some reproductive organs including testis and prostate. Hormonal analysis revealed that, TMX induced a significant elevation in the serum testosterone level, while the concentrations of FSH and LH hormones did not exhibit any alterations between treated and control groups. In addition, LDH-C4, FSHβ and LHβ and GnRHR genes were down regulated in TMX treated group. Conclusion: Administration of thiamethoxam for 90 days in male rabbits induced a noticeable adverse effect on serum testosterone level and down regulated genes related to male rabbit reproductive performance.

This study aims to see if Ginseng® can reduce the hepatorenal damage caused by malathion. Four groups of forty male Wistar albino rats were alienated. Group 1 was a control group that got orally supplied corn oil (vehicle). Group 2 was intoxicated by malathion dissolved in corn oil orally at 135 mg/kg/day. Group 3 orally received both malathion + Panax Ginseng® (300 mg/kg/day). Group 4 was orally given Panax Ginseng® at a 300 mg/kg/day dose. Treatments were administered daily and continued for up to 30 consecutive days. Malathion’s toxic effect on both hepatic and renal tissues was revealed by a considerable loss in body weight and biochemically by a marked increase in liver enzymes, LDH, ACP, cholesterol, and functional renal markers with a marked decrease in serum TP, albumin, and TG levels with decreased AchE and Paraoxonase activity. Additionally, malondialdehydes, nitric oxide (nitrite), 8-hydroxy-2-deoxyguanosine, and TNFα with a significant drop in the antioxidant activities were reported in the malathion group. Malathion upregulated the inflammatory cytokines and apoptotic genes, while Nrf2, Bcl2, and HO-1 were downregulated. Ginseng® and malathion co-treatment reduced malathion’s harmful effects by restoring metabolic indicators, enhancing antioxidant pursuit, lowering the inflammatory reaction, and alleviating pathological alterations. So, Ginseng® may have protective effects against hepatic and renal malathion-induced toxicity on biochemical, antioxidant, molecular, and cell levels.

This study aims to see if Ginseng

The current study was instigated by investigating the ameliorative potential of Ornipural

Increasing attention has been paid in the past decade to assessing the toxicological effects of nanoparticles and finding a protectant; thus, the current study aimed to investigate the protective effect of the mitochondria-targeting drug methylene blue (MB) against copper oxide nanoparticle (CuO-NP)-induced neurobehavioral toxicity in rats. For this purpose, twenty rats were allocated to four equal groups (n = 5). The negative control group received distilled water intraperitoneally (IP) and Tween 80 (10 %) orally. The CuO-NP group was given a dose of 100 mg/kg of CuO-NPs, administered orally, and the positive control group was treated with 1 mg/kg MB intraperitoneally (IP). The final group was concurrently exposed to CuO-NPs and MB for 14 consecutive days. At the end of the study, each group was neurobehaviorally blind tested relative to other experimental animals, then brain tissue markers were determined and a histopathological examination was conducted. The results showed that supplementation with CuO-NPs induced neurobehavioral alterations; increased Cu content in the brain; and enhanced lipid peroxidation (malondialdehyde [MDA]), protein peroxidation (protein carbonyl [PC]), and DNA oxidative damage (8-hydroxy-2-deoxyguanosine [8−OH-dG]) compared to other treatments. In addition, a decrease was noted in the mitochondrial dehydrogenases’ (aldehyde dehydrogenase 2 [ALDH2], and glutamate dehydrogenase [GDH]) activity in Cu-exposed rats. The histopathological findings revealed shrunken, pyknotic, and hypereosinophic cortical neurons and increased immune positive brown staining of caspase-3 protein, indicating apoptosis. Co-treatment with methylene blue ameliorated the neurotoxic effects of CuO-NPs; therefore, MB evidently had a powerful modulatory effect against the neurotoxicity of nano-Cu oxide via its antioxidant and mitochondrial protection properties.

The current study was instigated by investigating the ameliorative potential of Ornipural® solution against the hepato-renal toxicity of malathion. A total number of 35 male Wistar albino rats were divided equally into five groups. Group 1 served as control and received normal saline intraperitoneally. Group 2, the sham group, were administered only corn oil (vehicle of malathion) orally. Group 3 was orally intoxicated by malathion in corn oil at a dose of 135 mg/kg BW via intra-gastric gavage. Group 4 received malathion orally concomitantly with Ornipural® intraperitoneally. Group 5 was given Ornipural® solution in saline via intraperitoneal injection at a dose of (1 mL/kg BW). Animals received the treatment regime for 30 days. Histopathological examination revealed the harmful effect of malathion on hepatic and renal tissue. The results showed that malathion induced a significant decrease in body weight and marked elevation in the activity of liver enzymes, LDH, and ACP. In contrast, the activity of AchE and Paraoxonase was markedly decreased. Moreover, there was a significant increase in the serum content of bilirubin, cholesterol, and kidney injury markers. A significant elevation in malondialdehyde, nitric oxide (nitrite), and 8-hydroxy-2-deoxyguanosine was observed, along with a substantial reduction in antioxidant activity. Furthermore, malathion increased tumor necrosis factor-alpha, the upregulation of IL-1B, BAX, and IFN-β genes, and the downregulation of Nrf2, Bcl2, and HO-1 genes. Concurrent administration of Ornipural® with malathion attenuated the detrimental impact of malathion through ameliorating metabolic biomarkers, restoring antioxidant activity, reducing the inflammatory response, and improving pathologic microscopic alterations. It could be concluded that Ornipural® solution demonstrates hepatorenal defensive impacts against malathion toxicity at biochemical, antioxidants, molecular, and cellular levels.

Metal oxide nanoparticles (NPs) induce oxidative stress that can cause cellular toxicity. A natural antioxidant that can be used to protect tissues from oxidative stress is curcumin.In the present study, we evaluated the protective effect of curcumin nanoparticles (curcumin-NPs) against copper oxide nanoparticles (CuO-NPs)-mediated hepatorenal effects on behavioral performance, biochemical markers, antioxidants, inflammation, apoptosis, and histopathology in rats.Twenty Wistar adult male rats were randomly divided into four groups (n = 5); Group Ι served as a control, group ΙΙ was orally gavaged with curcumin-NPs (100 mg/Kg), group ΙΙI orally received CuO-NPs (100 mg/kg), and group ΙV received both CuO-NPs and curcumin-NPs orally for 14 days.Behavioral performance, biochemical markers, antioxidants, inflammatory mediators, and apoptotic gene expression were evaluated in addition to histopathological and immunohistochemical examination.The results revealed that rats exposed to CuO-NPs suffered from behavioral alterations and hepatic and renal damages, which indicated by a marked elevation of serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, urea, uric acid, and creatinine and a decline of total protein. Moreover, there was a significant downregulation in the expression of antioxidants genes, whereas inflammatory mediators expression were upregulated. The histopathological and immunohistochemical examination also corroborated these findings. In contrast, rats co-treated with curcumin-NPs exhibited better behavioral performance, biochemical profile, gene expression, histological architecture, and immunohistochemical staining results.These findings strongly indicated that curcumin-NPs exert significant protection against the behavioral and hepatorenal disorders induced by CuO-NPs toxicity by modulating oxidative stress regulators and gene expression.

Zinc phosphide (Zn3P2) is a widely used rodenticide which has the potential to cause high mortality if ingested. The present study was designed in order to explore the hepatic injury in broiler chicks that were acutely intoxicated with Zn3P2. For this purpose, a total number of 12 broiler Saso chicks were divided into two equal groups. Birds of the first group were exposed to 300ppm Zn3P2 via food. Hepatic damage of intoxicated birds was evaluated biochemically and histologically using the transmission electron microscope and subsequently compared with another healthy non-treated controls (second group). The serum activity of aspartate aminotransferase (AST) was significantly higher in those poisoned with Zn3P2, While, activities of both Alanine aminotransferase (ALT) and Alkaline phosphatase (ALP), as well as, zinc concentration of hepatic tissue did not represented a significant difference between treated and control birds. Histological examination revealed presence of numerous heterogenic shaped mitochondria in hepatocytes of non-treated birds. Glycogen deposits were also scattered in the form of large electron dense deposits. Kupffer cell was irregular in shape and had numerous pseudopods often projected into sinusoidal lumen. In hepatic cells of intoxicated birds, mitochondrial swelling with cristolysis, few glycogen deposits, vacuoles in the cytoplasm and shrunken darkly stained nuclei are the major ultra-structural changes which were detected. It was concluded that the mitochondria could be one of the main target in hepatocytes for the toxic effect of Zn3P2 in broiler chicks.

This study was designed to investigate neuro-behavioral, neuro-biochemical and neuro-morphological alterations induced by sub-acute toxicity of lead (Pb) in male Wistar rats as well as the assessment of the neuroprotective effect of thiamine hydrochloride against Pb-induced behavioral, biochemical and morphological neuro-alterations. For this purpose 24 male Wistar rats were randomly divided into 4 groups (n=6). Rats in the 1st group were treated with lead acetate orally at dose of 100 mg/kg b.wt. Animals in 2nd group were received leaded water orally + 100 mg/kg thiamine hydrochloride intraperitoneally. 3rd group were treated only with thiamine hydrochloride. 4th group was served as the control animals. Animals were exposed to treatments once daily for 7 consecutive days. Behavioral alterations were assessed by applying neurological tests as elevated plus-maze and Morris water maze. The main neurotransmission systems as cholinergic, adrenergic, serotonergic and GAB Aergic were evaluated in brain tissue homogenate. Morphological alterations was assessed histopathologically. Results revealed that, Pb exposure caused spatial learning and memory impairment, as well as a significant increase in the content of acetylcholine, serotonin and norepinephrine while the activity of acetylcholinesterase and GABA content showed a significant decrease. Hemorrhage in brain, mild perivascular edema and perivascular cuffing were the main pb-induced morphological alterations. Simultaneous administration of thiamine markedly ameliorated Pb-induced neurotoxicity which was indicated by comparatively better behavioral performance, alleviation of the neurotransmitters disturbances and decreased the severity of histopathological lesions. In conclusion, thiamine has been found to be extremely significant in the fighting of Pb-induced neuro-manifestations.

Thiamethoxam (TMX) is a non-mutagenic neonicotinoid insecticide that is widely used to combat different types of insects. The hepatotoxicity and carcinogenicity of TMX have been approved previously in mice but not in rats. However, the TMX-induced hepatotoxic and pro-carcinogenic effects on rabbits remain unclear. The present study elucidated the roles of oxidative stress, pro-inflammatory cytokines, and apoptosis-related genes in the hepatotoxic and carcinogenic effects of TMX on rabbits. Sixteen male rabbits were equally divided into two groups; eight rabbits orally treated with TMX at a dose of 250 mg/kg b.w for 90 successive days. Hepatotoxic effects of TMX were evidenced by attenuation of liver enzyme activities, elevation of bilirubin levels, and alterations in the hepatic architecture, including hepatocyte death by necrosis and apoptosis, lymphocyte infiltration and fibrosis. TMX induced oxidative stress, as evidenced by the significant increases in malondialdehyde levels and antioxidant enzyme (glutathione transferase and catalase) activities along with a decrease in glutathione levels. TMX also up-regulated the mRNA levels of interleukin-6 (1.6-fold) and B cell lymphoma-2 (1.8-fold) and down-regulated the mRNA level of the tumor necrosis factor-α (0.8-fold), indicating its effects on cell survival and proliferation through the inhibition of apoptosis. Interestingly, the elevated level of carcinoembryonic antigen and the appearance of ground glass-like hepatocytes suggested that TMX exerted a pro-carcinogenic effect. In conclusion, TMX exerts potentially hepatotoxic and pro-carcinogenic effects on rabbits by modulating oxidative/antioxidative status and pro-inflammatory cytokine production, inhibiting apoptosis and activating cell survival pathways.

The protective role of the probiotic Bactosac® in minimizing the negative oxidative stress and the biochemical and morphological alterations induced by sub-chronic exposure of broiler chicks to 2500 ppm lead (pb) acetate in drinking water for 5 consecutive weeks was evaluated. Results revealed that body weight in Pb acetate treated broiler chicks was significantly decreased (47 %). However, the co-administration of Bactosac® with Pb acetate succeeded to improve this percent to 19.62 % in comparison to control group. Also, antioxidants parameters of hepatic and renal tissues were significantly changed in Pb acetate exposed chicks, where the GSH concentration was significantly enhanced, while, GST and CAT activities, were significantly inhibited. Lipid peroxidation indicator MDA was also significantly increased. Activity of hepatic transaminases ALT and AST were significantly elevated in Pb acetate treated chicks while serum creatinine and blood urea showed no significant changes. The accumulation pattern of Pb in treated chicks revealed that the highest and significant concentration was recorded in bone (160 times), then kidneys (13 times), followed by Liver (2.2 times) and brain (1.6), while muscles showed the lowest (1.3 times) accumulation to Pb when compared to control values. Histopathological examination revealed presence of hepatocytic degeneration, necrosis and hemorrhages, as well as, vascular congestion of the inter tubular blood vessels, interstitial mononuclear cell infiltration, glomerular hypercellularity and some areas of inter tubular mononuclear cell infiltrations and aggregations in kidneys of pb-intoxicated birds. Concurrent treatment of Bactosac® with Pb acetate in drinking water of broiler chicks revealed a significant improvement of the previous antioxidant parameters, liver transaminases, accumulation pattern of Pb and morphological alterations. It is concluded that probiotics Bactosac® play an important and promising tool to prevent/reduce pb toxicity in broiler chicks.