Nephroprotective effect of vitamin D Against Levofloxacin-induced renal injury: an observational study.

The pathogenesis of kidney damage involves complicated interactions between vascular endothelial and tubular cell destruction. Evidence has shown that vitamin D may have anti-inflammatory effects in several models of kidney damage. In this study, we evaluated the effects of synthetic vitamin D on levofloxacin-induced renal injury in rats. Forty-two white Albino rats were divided into six groups, with each group comprising seven rats. Group I served as the control (negative control) and received intraperitoneal injections of normal saline (0.5 ml) once daily for twenty-one days. Group II and Group III were treated with a single intraperitoneal dose of Levofloxacin (50 mg/kg/day) and (100 mg/kg/day), respectively, for 14 days (positive control groups). Group IV served as an additional negative control and received oral administration of vitamin D3 (500 IU/rat/day) for twenty-one days. In Group V, rats were orally administered vitamin D3 (500 IU/rat/day) for twenty-one days, and intraperitoneal injections of Levofloxacin (50 mg/kg/day) were administered on day 8 for 14 days. Group VI received oral vitamin D3 supplementation (500 IU/rat/day) for twenty-one days, followed by intraperitoneal injections of Levofloxacin (100 mg/kg/day) on day 8 for fourteen days. Blood samples were collected to measure creatinine, urea, malondialdehyde, glutathione reductase, and superoxide dismutase levels. Compared to the positive control group, vitamin D supplementation lowered creatinine, urea, and malondialdehyde levels, while increasing glutathione reductase and superoxide dismutase levels. Urea, creatinine, and malondialdehyde levels were significantly (p<0.05) higher in rats administered LFX 50mg and 100mg compared to rats given (LFX + vitamin D). The main findings of this study show that vitamin D reduces renal dysfunction, suggesting that vitamin D has antioxidant properties and may be used to prevent renal injury.

Co-exposure of sulfur nanoparticles and Cu alleviate Cu stress and toxicity to oilseed rape Brassica napus L.

Experiments were performed to explore the impact of sulfur nanoparticles (SNPs) on growth, Cu accumulation, and physiological and biochemical responses of oilseed rape (Brassica napus L.) inoculated with 5 mg/L Cu-amended MS medium supplemented with or without 300 mg/L SNPs exposure. Cu exerted severe phytotoxicity and inhibited plant growth. SNPs application enhanced the shoot height, root length, and dry weight of shoot and root by 34.6%, 282%, 41.7% and 37.1%, respectively, over Cu treatment alone, while the shoot and root Cu contents and Cu-induced lipid perodixation as the malondialdehyde (MDA) levels in shoots and roots were decreased by 37.6%, 35%, 28.4% and 26.8%. Further, the increases in superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR) and glutathione S-transferase (GST) enzyme activities caused by Cu stress were mitigated in shoots (10.9%-37.1%) and roots (14.6%-35.3%) with SNPs addition. SNPs also positively counteracted the negative effects on shoot K, Ca, P, Mg, Mn, Zn and Fe contents and root K, Ca, Mg and Mn contents from Cu exposure alone, and significantly promoted the nutrients accumulation in plant. Additionally, in comparison with common bulk sulfur particles (BSPs) and sulfate, SNPs showed more positive effects on promoting growth in shoots (6.7% and 19.5%) and roots (10.9% and 15.1%), as well as lowering the shoot Cu content (40.1% and 43.3%) under Cu stress. Thus, SNPs application has potential to be a green and sustainable technology for increasing plant productivity and reducing accumulation of toxic metals in heavy metal polluted soils.

A study of effect of Centella asiatica on oxidative markers in the hippocampus of offsprings born to alcohol-fed pregnant rats and the correlation with their cognitive functions.

OBJECTIVES: Alcohol consumption causes several harmful effects on the organs, which is hugely understated. Many deformities occur in the fetus when pregnant mothers indulge in alcoholism. Alcohol is a known teratogen, hence organ formation, particularly development of parts brain critical for cognitive function may be affected. The oxidative brain damage also could contribute to reduced cognitive efficiency of brain exposed to alcohol. In this study, effect of Centella asiatica in relieving the oxidative brain damage in offspring of alcohol fed mother rats was evaluated. METHODS: In this study we fed alcohol (5 g/kg body weight, 30% w/v) to a group of pregnant Wistar rats during gestation period, and another group served as control. Four groups of rats (n = 6 each) were selected from the offspring of these mother rats. The groups were, control, positive (treated) control, untreated and treated from alcohol-fed mother. Their cognitive parameters were tested in water maze, shuttle box and compared. Further their oxidative status was evaluated by estimating malondialdehyde (MDA), protein carbonyl, total antioxidants and glutathione reductase (GSH) in hippocampus. RESULTS: The results suggested that there was significantly high cognitive performance in maze test and shuttle box memory retention in rats treated with C. asiatica water extract and the antioxidant levels were high in their hippocampus. CONCLUSIONS: The outcome of the study suggested that C. asiatica produced beneficial effects in reversing the alcohol induced brain damage in pregnancy.

Inhibition of cadmium-induced oxidative injury in rat primary astrocytes by the addition of antioxidants and the reduction of intracellular calcium.

Exposure of the brain to cadmium ions (Cd(2+)) is believed to lead to neurological disorders of the central nervous system (CNS). In this study, we tested the hypothesis that astrocytes, the major CNS-supporting cells, are resistant to Cd(2+)-induced injury compared with cortical neurons and microglia (CNS macrophages). However, treatment with CdCl(2) for 24 h at concentrations higher than 20 microM substantially induced astrocytic cytotoxicity, which also resulted from long-term exposure to 5 microM of CdCl(2). Intracellular calcium levels were found to rapidly increase after the addition of CdCl(2) into astrocytes, which led to a rise in reactive oxygen species (ROS) and to mitochondrial impairment. In accordance, preexposure to the extracellular calcium chelator EGTA effectively reduced ROS production and increased survival of Cd(2+)-treated astrocytes. Adenovirus-mediated transfer of superoxide dismutase (SOD) or glutathione peroxidase (GPx) genes increased survival of Cd(2+)-exposed astrocytes. In addition, increased ROS generation and astrocytic cell death due to Cd(2+) exposure was inhibited when astrocytes were treated with the polyphenolic compound ellagic acid (EA). Taken together, Cd(2+)-induced astrocytic cell death resulted from disrupted calcium homeostasis and an increase in ROS. Moreover, our findings demonstrate that enhancement of the activity of intracellular antioxidant enzymes and supplementation with a phenolic compound, a natural antioxidant, improves survival of Cd(2+)-primed astrocytes. This information provides a useful approach for treating Cd(2+)-induced CNS neurological disorders.

Spread of oxidative damage and antioxidative response through cell layers of tobacco callus after UV-C treatment.

Tobacco (Nicotiana tabacum L. cv. Petit Havana) callus cultures were exposed to UV-C high dose pulse-treatment (254 nm, 50 kJ m(-2), 1 h-treatment). After 6, 24 and 48 h from the end of the treatment, calli were cut transversally in two layers and oxidative damage (malondialdehyde [MDA] and hydrogen peroxide), non-enzymatic (radical scavenging antioxidants [RSA] and polyamines) and enzymatic antioxidants (ascorbate peroxidase [APX, EC 1.11.1.11], glutathione reductase [GR, EC 1.6.4.2], catalase [CAT, EC 1.11.1.6] and guaiacol peroxidase [GPX, EC 1.11.1.7]) were evaluated. At each time-point data referred to UV-C treated calli were compared to data of untreated ones (control). Despite of a strong increase of H2O2 content, a slight cellular damage was observed in both upper and lower layers 24 and 48 h after UV-C treatment. An activation first of non-enzymatic antioxidants and then of enzymatic antioxidants was detected in UV-C treated calli. In particular, RSA and putrescine (PUT) accumulated 6 h after UV-C treatment while APX, GR and GPX enzyme activities increased 24 h after UV-C irradiation. Catalase activity did not change. UV-C-induced oxidative stress and antioxidative response were observed also in cell layers not directly exposed to UV irradiation, indicating that a stress signal was transmitted to the whole mass of callus.

Biosynthesis of dimethyl selenide from sodium selenite in rat liver and kidney cell-free systems.

A pathway for the synthesis of dimethyl selenide from sodium selenite was studied in rat liver and kidney fractions under anaerobic conditions in the presence of GSH, a NADPH-generating system, and S-adenosylmethionine. Chromatography of liver or kidney soluble fraction on Sephadex G-75 yielded a Fraction C (30,000 molecular weight) which synthesized dimethyl selenide, but at a low rate. Addition of proteins eluting at the void volume (Fraction A) to Fraction C restored full activity. Fractionation of Fraction A on DEAE-cellulose revealed that its ability to stimulate Fraction C was associated with two fractions, one containing glutathione reductase and the other a NADPH-dependent disulfide reductase. It was concluded that Fraction C contains a methyltransferase acting on small amounts of hydrogen selenide produced non-enzymically by the reaction of selenite with GSH, and that stimulation by Fraction A results partly from the NADPH-linked formation of hydrogen selenide catalyzed by glutathione reductase present in Fraction A. Washed liver microsomal fraction incubated with selenite plus 20 mM GSH also synthesized dimethyl selenide, but addition of soluble fraction stimulated activity. A synergistic effect was obtained when liver soluble fraction was added to microsomal fraction in the presence of a physiological level of GSH (2 mM), whereas at 20 mM GSH the effect was merely additive. The microsomal component of the liver system was labile, had maximal activity around pH 7.5, and was exceedingly sensitive to NaAsO2 (93% inhibition by 10(-6) M arsenite in the presence of a 20,000-fold excess of GSH). The microsomal activity apparently results from a Se-methyltransferase, possibly a dithiol protein, that methylates hydrogen selenide produced enzymically by the soluble fraction or non-enzymically when a sufficiently high concentration of GSH is used.