Abstract

The effect of the antioxidant gallic acid (GA) on Pb toxicity in blood, liver and kidney was investigated in the present study. Rats Wistar received Pb nitrate (50 mg/Kg/day, i.p., 5 days) followed by GA (13.5 mg/Kg, p.o., 3 days) or a chelating agent (EDTA, 55 mg/Kg, i.p.). As result, Pb decreased body weight, hematocrit and blood δ-aminolevulinic acid dehydratase (ALA-D) activity. In addition, high Pb levels were observed in blood and tissues, together with increased (1) lipid peroxidation in erythrocytes, plasma and tissues, (2) protein oxidation in tissues and (3) plasma aspartate transaminase (AST) levels. These changes were accompanied by decreasing in antioxidant defenses, like superoxide dismutase (SOD) activity in tissues and catalase (CAT) activity and reduced glutathione (GSH) in liver. GA was able to reverse Pb-induced decrease in body weight and ALA-D activity, as well as Pb-induced oxidative damages and most antioxidant alterations, however it did not decrease Pb bioaccumulation herein as EDTA did. Furthermore, EDTA did not show antioxidant protection in Pb-treated animals as GA did. In conclusion, GA decreased Pb-induced oxidative damages not by decreasing Pb bioaccumulation, but by improving antioxidant defenses, thus GA may be promising in the treatment of Pb intoxications.

Abstract

The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats.

Abstract

Visual impairment is a global public health problem that needs new candidate drugs. Chrysanthemum is a traditional Chinese drug, famous for its eye-protective function, with an unclear mechanism of action. To determine how chrysanthemum contributes to vision, we identified, for the first time, the component of chrysanthemum, diosmetin (DIO), which acts in protecting the injured retina in an adriamycin (ADR) improving model. We observed that DIO could attenuate the apoptosis of retinal cells in Sprague–Dawley rats and verified this effect in cultured human retinal pigment epithelium (RPE) cells, ARPE-19. Our further study on the mechanism revealed the counteractive effect of DIO on the attenuation of DNA damage and oxidative stress, which occurs in a wide range of retinal disorders. These results collectively promise the potential value of DIO as a retinal-protective agent for disorders that lead to blindness. In addition, we identified, for the first time, the component of chrysanthemum, DIO, which acts in protecting the injured retina.

Abstract

Redox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are deficient with aging and cellular senescence, leading to redox imbalance and oxidative stress. However, the precise mechanisms by which redox signaling and oxidative stress contribute to the pathogenesis of lung fibrosis are not well understood. Tissue repair is a highly regulated process that involves the interactions of several cell types, including epithelial cells, fibroblasts and inflammatory cells. Fibrosis may develop when these interactions are dysregulated with the acquisition of pro-fibrotic cellular phenotypes. In this review, we explore the roles of redox mechanisms that promote and perpetuate fibrosis in the context of cellular senescence and aging.

Abstract

Clinoptilolite is a natural zeolite crystal. Cytoprotective effects of clinoptilolite have been reported. However, so far there are no data about the effects of clinoptilolite treatment on oxidative stress after partial hepatectomy. In this experimental study, the effects of clinoptilolite treatment after partial hepatectomy on oxidative stress were evaluated. There were four experimental groups (n = 8): Group S, the sham group, Group H, the hepatectomy group, Group HC, the clinoptilolite treatment after partial hepatectomy group, and Group CS, the clinoptilolite-treated sham group. A 70% partial hepatectomy was performed for Group H and HC. Clinoptilolite (5 mg/kg) was given to the rats orally (via gavage tube) twice a day for 10 days after hepatectomy. Malondialdehyde (MDA), Cu-Zn super oxide dismutase (SOD), and glutathione (GSH) levels were assessed to evaluate oxidative stress. Plasma and liver tissue MDA levels of Group HC were significantly lower than the H group (p = 0.018 and p = 0.000, respectively). Liver tissue Cu-Zn SOD activity and GSH levels of Group HC were significantly higher than Group H (p = 0.003, p = 0.007, respectively). Clinoptilolite administration reduces oxidant activity and supports antioxidant response after partial hepatectomy.

Abstract

To observe the effects of intermittent one-lung ventilation (OLV) before and after surgery on the inflammatory cytokines and biomarkers of oxidative stress in serum of lung cancer patients undergoing open thoracotomy. Between June 2011 to March 2012, 80 patients undergoing lobectomy were classified into four groups nonrandomly: Group A, control group, B, OLV preconditioning group, C, OLV postconditioning group, D, OLV preconditioning-combined-with-postconditioning group. Neutrophil granulocyte (PMN), interleukin 6 (IL-6), superoxide dismutase (SOD), and malondialdehyde (MDA) were assayed in plasma samples taken preoperatively (T1), intraoperatively (T2), and 2 hours postoperatively (T3). Comparison of T1 with T2 and T3 documented significant increase in MDA, PMN, and IL-6 levels and decrease in SOD in the control group (p < 0.01). Compared with the control group, the levels of IL-6 and MDA decreased and SOD increased significantly at T2 in the OLV preconditioning group, at T3 in the OLV preconditioning combined postconditioning group (p < 0.05). Preconditioning of intermittent OLV before thoracotomy combined with postconditioning of intermittent returning two-lung ventilation after surgery maybe alleviate systematic inflammatory response and oxidative stress for lung cancer patients.

Abstract

The study aims to evaluate the alterations in the brain due to oxidative stress and lipid peroxidation resulting from obstructive jaundice. Forty-one Wistar albino rats were used in this study. Simple laparotomy was performed in the sham group (n = 5). In the remaining 36 rats, the common bile duct (CBD) was found and ligated. They were divided into six groups. Group I, Group II, and Group III were sacrificed at the 3rd, 7th, and 14th day of ligation, respectively. In Group Id, Group IId, and Group IIId ligated bile ducts were decompressed at the 3rd, 7th, and 14th day, respectively. One week after decompression these rats were also sacrificed and samples were taken. After the CBD ligation, serum levels of bilirubin and malondialdehyde were found to be increased progressively in parallel to the ligation time of the CBD. After decompression these values decreased. In electron microscopy evaluation, the damage was found to be irreversible depending on the length of the obstruction period. In Group II, the damage was mostly reversible after the internal drainage period of 7 days. However in Group III, the tissue damage was found to be irreversible despite the decreased values of oxidative stress and bilirubin. Ultrastructural changes in brain tissue including damage in the glial cells and neurons, were found to be irreversible if the CBD ligation period was >7 days and did not regress even after decompression. It is unreliable to trace these changes using blood levels of bilirubin and free radicals. Therefore, timing is extremely critical for medical therapies and drainage.

Abstract

This study was designed to test the hypothesis that supplementation with vitamin E, an antioxidant, in cats with chronic kidney disease (CKD), would reduce oxidative stress and its impact on RBC membrane fragility, resulting in these cats maintaining a greater packed cell volume (PCV) compared with CKD cats not receiving supplementation. Thirty-six cats with CKD were randomly assigned to receive either daily vitamin E or a placebo for 3 months in a double-blinded study design. History and physical examination, blood pressure, complete blood count (CBC), PCV, biochemical profile and urinalysis (UA) were determined. Parameters of oxidative stress and osmotic fragility were measured. Cats were administered vitamin E or placebo once daily for 3 months. Cats were then reassessed and the diagnostics were repeated. Twenty-four cats completed the study, 11 in the vitamin E group and 13 in the placebo group. There were no significant differences between the two groups at the start, or upon completion of the study with regard to biochemical parameters, oxidative stress, erythrocyte osmotic fragility or PCV. None of these parameters changed significantly in either group over the treatment period. Daily supplementation with 30 IU of vitamin E did not affect the measures of oxidative stress or the anaemia seen in cats with CKD.

Abstract

Age-related hearing loss (AHL), or presbycusis, is the most common neurodegenerative disorder and top communication deficit of the aged population. Genetic predisposition is one of the major factors in the development of AHL. Generally, AHL is associated with an age-dependent loss of sensory hair cells, spiral ganglion neurons and stria vascularis cells in the inner ear. Although the mechanisms leading to genetic hearing loss are not completely understood, caspase-family proteases function as important signals in the inner ear pathology. It is now accepted that mouse models are the best tools to study the mechanism of genetic hearing loss or AHL. Here, we provide a brief review of recent studies on hearing improvement in mouse models of AHL by anti-apoptotic treatment.

Abstract

Cancer is a complex disease marked by uncontrolled cell growth and invasion. These processes are driven by the accumulation of genetic and epigenetic alterations that promote cancer initiation and progression. Contributing to genome changes are the regulation of oxidative stress and reactive species-induced damage to molecules and organelles. Redox regulation, metabolic plasticity, autophagy, and mitophagy play important and interactive roles in cancer hallmarks including sustained proliferation, activated invasion, and replicative immortality. However, the impact of these processes can differ depending on the signaling pathways altered in cancer, tumor type, tumor stage, and/or the differentiation state. Here, we highlight some of the representative studies on the impact of oxidative and nitrosative activities, mitochondrial bioenergetics, metabolism, and autophagy and mitophagy in the context of tumorigenesis. We discuss the implications of these processes for cellular activities in cancer for anti-cancer-based therapeutics.