Ziziphus spina-christi leaf extract attenuates mercury chloride-induced testicular dysfunction in rats.

Mercury (Hg) is a heavy metal toxicant, causing several adverse reactions to animals and humans including reproductive dysfunction. The potential protective role of Ziziphus spina-christi leaf extract (ZSCLE) against testicular impairments associated with mercury chloride (HgCl2) exposure in rats was investigated in the current study. Four experimental groups were employed as follows (n = 7): group I served as control, group II was gavaged with ZSCLE (300 mg/kg), group III was administered with HgCl2 (0.4 mg/kg), and group IV was preadministered with ZSCLE 1 h before HgCl2. All groups were treated daily for 28 days. The exposure to HgCl2 caused a marked increase in Hg concentration in the testicular tissue, which was accompanied with a decrease in testis index. A reproductive impairment was recorded following HgCl2 exposure as verified through the decrease in levels of testosterone, luteinizing, and follicle-stimulating hormones. HgCl2 was found to enhance the development of oxidative damage in the testicular tissue as presented by the imbalance between pro-oxidants and antioxidant molecules. In addition, excessive release of tumor necrosis factor-α and interleukin-1ß was recorded in response to HgCl2 intoxication. Furthermore, a disturbance in the apoptotic proteins in favor of the pro-apoptotic proteins was also observed following HgCl2 intoxication. However, ZSCLE administration along with HgCl2 abolished significantly the molecular, biochemical, and histopathological alterations induced by HgCl2 intoxication. Our findings suggest that ZSCLE could be used to mitigate reproductive dysfunction associated with HgCl2 exposure.

The effect of ferulic acid against lead-induced oxidative stress and DNA damage in kidney and testes of rats.

Oxidative stress is an imbalance between free radicals and antioxidants which leads to reactive oxygen species (ROS) production in cells. Reactive oxygen species contains oxygen radicals that easily react with other molecules in the biological system. For decades, lead acetate (Pb(C2H3O2)2) is used as an additive for many widely used chemical products such as insecticides, hair dyes, and cosmetics; however, contact with lead acetate may irritate skin, eyes, and mucous membranes.In the present study, the antioxidant and anti-inflammatory effect of using ferulic acid to inhibit lead acetate-induced toxicity in rats is investigated. Lead acetate was orally given at a dose of 20 mg/kg body weight for 10 days, either alone or with ferulic acid at dose 25 mg/kg. Serum luteinizing hormone (LH), total testosterone, and follicle-stimulating hormone (FSH) levels were measured. Also, reactive oxygen species (ROS), lipid peroxidation (LPO), total antioxidant capacity (TAC), and catalase (CAT) activities were determined. In addition, histopathological changes of testes and kidney were examined. Results showed that administration of lead acetate induced oxidative stress through attenuation of luteinizing hormone, total testosterone, and follicle-stimulating hormone levels in serum. Moreover, the kidney and testes of lead acetate-treated animals exhibited elevation of ROS level, lipid peroxide levels, as well as lysosomal enzyme activity such acid phosphatase and N-acetyl-ß-glucosminidase. DNA fragmentation and histological changes were also observed in lead acetate-treated group. In contrast, ferulic acid treatment reduced the deleterious effects induced by lead acetate in both testes and kidney tissues. These results illustrated that ferulic acid has a protective action against toxicity caused by lead acetate in rats. In conclusions, ferulic acid may have future therapeutic relevance in the prevention of lead acetate-induced testicular and renal toxicity in rats.

The potential hepatoprotective effect of royal jelly against cadmium chloride-induced hepatotoxicity in mice is mediated by suppression of oxidative stress and upregulation of Nrf2 expression.

This study was aimed at investigating the possible protective mechanism of royal jelly (RJ) against hepatotoxicity induced by cadmium chloride (CdCl2). The study included four groups: the control group received saline (0.9% sodium chloride), CdCl2 group received 6.5 mg/kg CdCl2 for seven days, RJ group received 85 mg/kg standardized RJ containing 6% 10-hydroxy-2-decenoic acid equivalent to 250 mg crude RJ, and finally, the fourth group received RJ 2 h before CdCl2 injection daily for 7 days. Oxidant/antioxidant markers of liver function estimation and histopathology were determined. The results revealed that RJ significantly ameliorated the hepatotoxic side effects of Cd. Furthermore, RJ inhibited oxidative stress, inflammation, and hepatic tissue injury; normalized enzymatic and nonenzymatic antioxidant molecules; and enhanced nuclear-related factor-2 (Nrf-2) expression. Our results provide new insights into the hepatoprotective property of RJ and revealed that RJ prevented hepatic injury, oxidative stress, and inflammation by upregulating Nrf2 and the anti-apoptotic protein Bcl-2. Hence, RJ can be used as a hepatoprotective agent against the toxic effects of CdCl2.

Ceratonia siliqua pod extract ameliorates Schistosoma mansoni-induced liver fibrosis and oxidative stress.

BACKGROUND: Schistosomiasis is a prevalent parasitic disease found predominantly in tropical and sub-tropical areas of the developing world, with the second highest socioeconomic and public health burden despite strenuous control efforts. In the present study, we aimed to investigate the ameliorative effects of Ceratonia siliqua pod extract (CPE) on liver fibrosis and oxidative stress in mice infected with Schistosoma mansoni. METHODS: The schistosomal hepatopathologic mouse model was established by tail immersion with schistosomal cercaria. The extract was given daily for 10 days beginning 42 days post-infection. Liver samples were obtained from mice sacrificed 9 weeks after infection. Liver histopathological changes were observed with hematoxylin-eosin and Masson trichrome staining. RESULTS: Typical schistosomal hepatopathologic changes were induced in the untreated mice. However, the oral administration of CPE was effective in reducing worm number and the egg load in the liver. This treatment also decreased granuloma size and collagen deposition by inhibiting tissue inhibitor of metalloproteinases-2 (TIMP-2) expression. Schistosomal infection induced oxidative stress by increasing lipid peroxidation (LPO) and nitrite/nitrate (nitric oxide; NO) production along with concomitant decreases in glutathione (GSH) and various antioxidant enzymes, including superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. However, treatment of mice with CPE at 300 or 600 mg/kg inhibited LPO and NO production, increased GSH content, and restored the activities of the antioxidant enzymes compared with untreated infected mice. Furthermore, treatment with CPE inhibited apoptosis, as indicated by the reduced Bax expression in hepatic tissue. CONCLUSION: These data indicated that extracts from Ceratonia siliqua pods may play an important role in combating schistosomal hepatopathology and may inhibit granuloma formation and liver fibrosis through down-regulation of TIMP-2 expression.

Neuroprotective potential of Indigofera oblongifolia leaf methanolic extract against lead acetate-induced neurotoxicity.

Lead (Pb) is one of the most common environmental toxicants, exposure to which can cause significant neurotoxicity and an associated decline in brain function. This study investigated the possible neuroprotective role of Indigofera oblongifolia leaf methanolic extract (IOLME) against lead-induced neurotoxicity. Rats were intraperitoneally injected with lead acetate, with or without IOLME (intragastric administration for 5 days), and the neuroprotective effect of IOLME was assessed by measuring the lead concentration, redox status (lipid peroxidation, nitric oxide and glutathione), enzymatic antioxidant activities (superoxide dismutase, catalase, glutathione peroxidase and reductase), PCR assays of apoptosis markers (Bax and Bcl-2) and histopathology of the brain. The increases in the lipid peroxidation, nitric oxide, and apoptosis, the decreases in the glutathione level and the activity of antioxidant enzymes, and the altered histology of the brain induced by lead acetate were mitigated in the brain of rats pre-treated with IOLME. These findings indicate that IOLME has beneficial effects and it mitigates lead acetate-induced neurotoxicity via its antioxidant and anti-apoptotic activities.