Antioxidant effects of propolis on carp Cyprinus carpio exposed to arsenic: biochemical and histopathologic findings.

Propolis, a resinous material produced by worker bees from the leaf buds and exudates of plants, is reported to possess various therapeutic properties. The aim of this study was to investigate the effects of propolis on biochemical parameters and histopathologic findings in carp Cyprinus carpio L. exposed to arsenic. A sublethal concentration of arsenic (0.01 mg l-1) and/or 10 mg l-1 propolis were administered to fish for 1 wk. Catalase (CAT) activities and malondialdehyde (MDA) levels were determined in liver, gill and muscle tissues in control, arsenic only, propolis only and arsenic+propolis treatment groups. Results showed that CAT activity decreased in the arsenic group compared to the control and propolis groups. CAT activity in the arsenic+propolis group was significantly higher compared to the arsenic group. MDA levels in fish exposed to 0.01 mg l-1 arsenic significantly increased compared to the control group. However, MDA levels in the arsenic+propolis group were significantly lower compared to the arsenic group. Histopathological changes in the liver, gill and muscle tissues of carp were examined by light microscopy: various changes were observed in all tissues of fish in the arsenic group. Propolis showed important antioxidant effects against arsenic toxicity in all fish tissues.

Antioxidative role of selenium on some tissues of (Cd2+), Cr3+)-induced rainbow trout.

Chemical toxic pollutants (especially heavy metals) are important sources of reactive oxygen species (ROS) in biological systems. Membrane phospholipids of aerobic organisms are continually subjected to oxidant challenges from endogenous and exogenous sources, while peroxidized membranes and lipid peroxidation products represent constant threats to aerobic cells. The primary antioxidant protection against free radical and ROS is provided by the enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT), respectively. The trace element selenium has been implicated in chemo-prevention and drug-resistance through reduction of oxidative stress. Selenium could prevent damage to the unsaturated fatty acid of subcellular membranes by lipid peroxidation induced by free radicals. The results reported here show that sodium selenite has an important contribution to antioxidative defense for the spleen and heart of rainbow trout. The ability of sodium selenite to prevent the oxidative stress induced by heavy metals (Cd(2+), Cr(3+)) in fish was rationalized.

Antioxidative role of selenium against the toxic effect of heavy metals (Cd+2, Cr+3) on liver of rainbow trout (Oncorhynchus mykiss Walbaum 1792).

The main purpose of this study is to discuss the effect of Cd+2, Cr+3 and Se metals on biochemical parameters in liver tissue of Oncorhynchus mykiss. The rainbow trout were exposed to heavy metal stress (Cd+2, Cr+3) at 2 ppm dosage. The present study was undertaken to determine the protective effect of selenium treatment at the same dosage (2 ppm) on some biochemical parameters. The activity of catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and the changes in levels of malondialdehyde (MDA) from biochemical parameters were determined in liver tissue of the fish groups exposed to heavy metals, especially for the selenium-applied groups. Results of this study showed that the activities of CAT, GSH-Px and SOD in the tissues of fish exposed to the stress of Cd+2 and Cr+3 were significantly lower than the control groups (P < 0.05). Meanwhile, the closer values to the control groups were obtained in selenium-added groups (Cr+3 + Se+4, Cd+2 + Se+4). For the level of MDA, the last production of lipid peroxidation showed increases (P < 0.05) in the groups exposed to the metal stress, whereas significant decreases were obtained in selenium-applied groups. The result of the statistical evaluation showed that the negative effects occurring in the biochemical parameters of the applied groups exposed to the toxicity of heavy metal were significantly eliminated (P < 0.05) as a result of selenium treatment.

The effects of chronic exposure to ethanol and cigarette smoke on the formation of peroxynitrite, level of nitric oxide, xanthine oxidase and myeloperoxidase activities in rat kidney.

The aim of this study was to investigate the effects of chronic ethanol intake and cigarette smoke exposure on rat kidney. The animals were divided into four experimental groups: (1) the control group (C), (2) the ethanol group (E), (3) the cigarette smoke group (CS), and (4) the cigarette smoke plus ethanol group (CS+E). Rats in E, CS and CS+E groups were treated with ethanol and/or cigarette smoke for 6 months. The animals were killed and the kidneys were removed to determine the activity of xanthine oxidase (XO), myeloperoxidase (MPO) and the levels of nitric oxide (NO). Histopathological and immunohistochemical analysis were performed in kidney tissues. The activity of XO/g protein were 2.8 +/- 0.3, 5.2 +/- 0.3, 3.2 +/- 0.1, and 7.4 +/- 0.7 U for C, E, CS and CS+E groups, respectively. In groups E, and CS+E, the XO values were significantly higher than in group C (P < 0.05). The increase in XO activity of CS was not significantly different from group C (P > 0.05). There was a significant increase in XO activity of group CS+E as compared to CS and E groups (P < 0.05), and also a significant difference in XO activity between E and CS was observed (P < 0.05). The activity of MPO/g protein were 13.5 +/- 0.6, 16.2 +/- 1.1, 14.7 +/- 1.1, 23.8 +/- 0.9 U for C, E, CS, and CS+E groups, respectively. While MPO activity of kidneys from group CS+E were significantly higher as compared to C, CS, and E groups (P < 0.05), there was no significant difference among the groups of C, CS, E (P > 0.05). The levels of NO/g wet tissue were 347.7 +/- 8.5, 261.1 +/- 4.8, 329.8 +/- 5.6, and 254.2 +/- 3.8 nmol for C, E, CS, and CS+E groups, respectively. In groups of E and CS+E, the NO values were significantly lower than that of group C animals (P < 0.05). Although we detected lower NO levels in the E and CS+E groups than in CS group (P < 0.05), a significant difference in NO levels between CS+E and E groups was not observed. In the histopathological analysis of the kidney slices, severe degenerations in kidney tissues of group CS, E, CS+E were observed. Generally, the histological changes in kidney of CS+E and E groups were more severe than those observed in CS alone. While we observed a strong immunoreactivity for anti-nitrotyrosine antibody in kidneys of group CS+E, examination of sections from rat kidneys in group E revealed moderate staining. On the other hand, group CS had very little immunostaining. There was no immunostaining in group C. We concluded that chronic ethanol administration and cigarette smoke exposure may cause oxidative and nitrosative stress which lead to rat kidney damage.