Ziziphus spina-christi leaf extract attenuates mercuric chloride-induced liver injury in male rats via inhibition of oxidative damage

Environmental Science and Pollution Research - Heavy metal contamination including mercury (Hg) has become one of the most serious environmental problems facing humans and other living organisms....     

Histological and histochemical alterations induced by lead in the liver of the quail Coturnix coturnix

Adult males of the quail Coturnix coturnix were exposed to lead acetate trihydrate in drinking water (0.1, 0.25, 0.5, and 1% for one–six months) to investigate histological and histochemical alterations induced by lead intoxication in the liver. Chronic exposure to subtoxic concentrations of lead produced changes in hepatocytes, portal veins, Kupffer cells, and blood sinusoids. Alterations in hepatocytes mainly involved cytoplasmic vacuolation, necrosis, cytolysis, and glycogen accumulation. Kupffer cell hyperplasia, hemosiderosis, blood sinusoidal dilatation, portal vein congestion, and edema were also observed. No fibrosis or cirrhosis in the liver of any member of the dose groups over the entire period of the study was noted. The findings revealed that chronic exposure to lead produced mild histological and histochemical changes in the liver of the quail Coturnix coturnix.     

The ameliorative effects of ceftriaxone and vitamin E against cisplatin-induced nephrotoxicity

Environmental Science and Pollution Research - Nephrotoxicity is a common adverse effect of treatment with cisplatin (CDDP). This study was performed to evaluate the antioxidant and...     

Determination of nephrotoxicity and genotoxic potential of silver nanoparticles in Swiss albino mice

Silver nanoparticles (AgNPs) possess properties that are important for industrial and medical applications. This study is aimed to investigate intra-peritoneal toxicity of AgNPs at 26, 52 or 78 mg/kg/day for 5 days in mice Swiss albino mice. The effects on oxidative stress markers activities of serum superoxide dismutase (SOD) and catalase (CAT), levels of serum glutathione (GSH), apoptosis (TUNEL assay), DNA strand breaks (comet assay) in lymphocytes, as well as histopathological of kidney tissue were determined. AgNPs significantly increased SOD and CAT activities reduced GSH levels. In kidney apoptosis (TUNEL assay) while DNA strand breaks (comet assay) in lymphocytes revealed that AgNPs at concentration 78 mg/kg produced significant apoptosis and DNA damage. AgNPs also produced associated histological renal tissue damage. Evidence suggests that AgNPs-mediated alterations may be attributed to oxidative stress.     

Involvement of mitochondrial dysfunction in nanosized lead oxide induced cellular damage in human lung alveolar epithelial cells

High levels of industrial lead (Pb) exposure have decreased in the last 10 years as an outcome of removal of the metal from gasoline and paints. However, environmental Pb exposures remain extensive and may be correlated with adverse human health outcomes. The present study was designed to examine molecular mechanisms underlying cytotoxicity of lead oxide nanoparticles (PbONPs) on human lung alveolar epithelial (A549) cells. When A549 cells were incubated with PbONPs, the production of reactive oxygen species was enhanced as observed by 2',7'-dichlorodihydrofluorescein diacetate. PbONPs significantly reduced proliferation of A549 cells and increased caspase3 activity. In addition, exposure of PbONPs decreased levels of glutathione, and increased lipid peroxide levels and activities of superoxide dismutase and catalase. Exposure of PbONPs enhanced DNA damage as evidenced by tail DNA (%) and olive tail moment. Taken together, these finding indicated that PbONPs diminished cell proliferation and increased apoptotic cell death of A549 cells.     

Genotoxicity in the freshwater gastropod Lymnaea luteola L: assessment of cell type sensitivities to lead nitrate

The aquatic ecosystems are converting into the highly contaminated site due to environmental pollutants. The present study explores the oxidative stress and toxic potential of lead nitrate in freshwater snail Lymnaea luteola (L. luteola) L. The snails were exposed to an environmentally relevant concentration of lead nitrate for 24 and 96?h. Later exposure to lead nitrate (0, 10, 20 and 40?µg/mL) to the freshwater snail, the level of reactive oxygen species, malondialdehyde and nitric oxide (NO) were increased and glutathione, glutathione-S-transferase were decreased. Lead-nitrate-induced haemocyte cell death and it was observed by using Annexin-V FITC/PI through a flow cytometer. DNA damage in haemocyte cells was measured at above doses of lead-nitrate exposure for 24 and 96?h and it was compared to the untreated snail. Average tail DNA (%) and olive tail moment in single-cell gel test were increased dose and duration fashion and maximum DNA damage was measured at 96?h. These results indicate the potential toxicity and genotoxicity of lead nitrate in acute treatment to L. luteola and single-cell gel test are the assay for rapid detection of genetic effects.