Production and properties of α-amylase from Bacillus sp. BKL20

As a result of screening Bacillus sp. strains isolated from different natural substrates, strain BKL20 was identified as a producer of a thermostable alkaline α-amylase. Maximum production of this α-amylase was achieved by optimizing culture conditions. Production of α-amylase seemed to be independent of the presence of starch in the culture medium and was stimulated by the presence of peptone (0.3%, m/v) and yeast extract (0

Low toxic herbicide Roundup induces mild oxidative stress in goldfish tissues

The formulation of Roundup consists of the herbicide glyphosate as the active ingredient with polyethoxylene amine added as a surfactant. The acute toxicity of Roundup (particularly of glyphosate) to animals is considered to be low according to the World Health Organization, but the extensive use of Roundup may still cause environmental problems with negative impact on wildlife, particularly in an aquatic environment where chemicals may persist for a long time. Therefore, we studied the effects of Roundup on markers of oxidative stress and antioxidant defense in goldfish, Carassius auratus. The fish were given 96 h exposure to Roundup at concentrations of 2.5-20 mg L-1. Exposure to Roundup did not affect levels of lipid peroxides (LOOH) in goldfish brain or liver, and in kidney only the 10 mg L-1 treatment elevated LOOH by 3.2-fold. Herbicide exposure also had no effect on the concentrations of protein thiols or low molecular mass thiols in kidney, but selective suppression of low molecular mass thiols by 26-29% occurred at some treatment levels in brain and liver. Roundup exposure generally suppressed the activities of superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione reductase and glucose-6-phosphate dehydrogenase in fish tissues. For example, SOD activities were reduced by 51-68% in brain, 58-67% in liver and 33-53% in kidney of Roundup treated fish. GST activity decreased by 29-34% in liver. However, catalase activity increased in both liver and kidney of herbicide-exposed fish. To our knowledge this is the first study to demonstrate a systematic response by the antioxidant systems of fish to Roundup exposure

The effect of potassium dichromate on free radical processes in goldfish: Possible protective role of glutathione

The effects of 96 h exposure to Cr6+ (added as potassium dichromate) on the status of antioxidant defenses and markers of oxidative damage were evaluated in three tissues of goldfish, Carassius auratus. Fish exposure to high dichromate concentrations, 10 and 50 mg/l, increased protein carbonyl levels in brain and liver, but not in kidney. Chromium exposure also increased concentrations of lipid peroxides in brain (at 5 mg/l) and liver (10 mg/l), but not in kidney. The concentrations of reduced glutathione (GSH) were higher in the liver of goldfish treated with 5-50 mg/l Cr6+ than in controls, but in kidney only the 5 mg/l-treated group showed increased GSH levels. Dichromate at 1 mg/l increased the concentration of oxidized glutathione (GSSG) in liver and kidney by 80% and 60%, respectively, whereas at 10 and 50 mg/l the levels of GSSG decreased by 50% in kidney. These results indicate that the dichromate concentrations used induced oxidation of lipids and proteins in goldfish tissues in a concentration- and tissue-specific manner. Also, the redox status of fish tissues was affected in a concentration- and tissue-specific manner. The activities of glutathione reductase increased in all three tissues in response to dichromate treatment, increasing by ∼2-fold in brain and liver in goldfish treated with 50 mg/l Cr6+. Dichromate treatment did not change the activities of SOD, catalase or GST in brain, but reduced the activities of SOD in liver and kidney, and catalase in liver. The results suggest that the glutathione system may be responsible for protecting against the deleterious effects of dichromate in fish and indicate the possible development of an adaptive response during the 96 h treatment with the toxicant

Trivalent chromium induces oxidative stress in goldfish brain

Although information on the effects of Cr6+ in biological systems is abundant, Cr3+ has received less attention. Toxic effects of chromium compounds are partially associated with activation of redox processes. Recently we found that Cr6+ induced oxidative stress in goldfish tissues and the glutathione system was shown to play a protective role. The present study aimed to investigate free radical processes in brain of goldfish exposed to CrCl3. Trivalent chromium at a concentration of 50 mg L-1 was lethal and therefore we chose to examine sublethal dosages of 1.0-10.0 mg L-1 in aquarium water. The levels of lipid peroxides and protein carbonyls (measures of oxidative damage to lipids and proteins) in brain increased after 96 h exposure of goldfish to Cr3+. However, exposure to 1.0-10.0 mg L-1 Cr3+ decreased total glutathione concentration in brain by ∼50-60%. Oxidized glutathione levels also fell by ∼40-60% except at the 10.0 mg L-1 dosage where they decreased by 85%. Therefore, 10.0 mg L-1 Cr3+ significantly reduced the ratio [GSSG]/[totalGSH] to 35% of the control value. Chromium treatment did not affect the activity of superoxide dismutase, but reduced the activities of catalase by 55-62% and glutathione-S-transferase by 14-21%. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were unchanged under any experimental conditions used. Therefore, it can be concluded that although Cr3+ exposure induced oxidative stress in goldfish brain, it failed to enhance the efficiency of the antioxidant system in the organ

Chromium(III) induces oxidative stress in goldfish liver and kidney

In the environment chromium is found mainly in two valence states-hexavalent chromium (Cr6+) and trivalent chromium (Cr3+). The present study evaluates the effects of Cr3+ exposure on goldfish by analyzing parameters of oxidative stress and antioxidant defense in liver and kidney of fish given 96 h exposures to Cr3+ concentrations of 1, 2.5, 5 or 10 mg/l in aquarium water. Cr3+ exposure did not alter two parameters of oxidative stress-protein carbonyl content and lipid peroxide concentrations in either organ. However, Cr3+ exposure did decrease total glutathione concentration in liver by 34-69% and in kidney to 36-49% of the respective control values. Oxidized GSSG content fell by similar percentages so that the ratio [GSSG]/[total glutathione] remained constant at all Cr3+ exposure levels except in liver under the highest, 10 mg/l, exposure level. In liver, exposure to 1-5 mg/l Cr3+ led to a decrease in the activity of superoxide dismutase (SOD) by 29-36%, and at 10 mg/l Cr3+ the reduction was 54%, whereas in kidney ∼30% reductions in SOD activity were seen at concentrations 1 and 10 mg/l Cr3+. Catalase activity was not significantly affected by 1-5 mg/l Cr3+, but was reduced by 57 and 42% in liver and kidney, respectively. Chromium exposure also reduced the activity of glutathione-S-transferase in both organs by 17-50% but did not affect glutathione reductase or glucose-6-phosphate dehydrogenase activities. A comparison of Cr3+ effects on goldfish liver and kidney metabolism indicates that the trivalent ion induces stronger oxidative stress than Cr6+ at the same concentrations

Cobalt-induced oxidative stress in brain, liver and kidney of goldfish Carassius auratus

Cobalt is an essential element, but at high concentrations it is toxic. In addition to its well-known function as an integral part of cobalamin (vitamin B 12), cobalt has recently been shown to be a mimetic of hypoxia and a stimulator of the production of reactive oxygen species. The present study investigated the responses of goldfish, Carassius auratus, to 96h exposure to 50, 100 or 150mgL -1 Co 2+ in aquarium water (administered as CoCl 2). The concentrations of cobalt in aquaria did not change during fish exposure. Exposure to cobalt resulted in increased levels of lipid peroxides in brain (a 111% increase after exposure to 150mgL -1 Co 2+) and liver (30-66% increases after exposure to 50-150mgL -1 Co 2+), whereas the content of protein carbonyls rose only in kidney (by 112%) after exposure to 150mgL -1 cobalt. Low molecular mass thiols were depleted by 24-41% in brain in response to cobalt treatment. The activities of primary antioxidant enzymes, superoxide dismutase (SOD) and catalase, were substantially suppressed in brain and liver as a result of Co 2+ exposure, whereas in kidney catalase activity was unchanged and SOD activity increased. The activities of glutathione-related enzymes, glutathione peroxidase and glutathione-S-transferase, did not change as a result of cobalt exposure, but glutathione reductase activity increased by ∼40% and ∼70% in brain and kidney, respectively. Taken together, these data show that exposure of fish to Co 2+ ions results in the development of oxidative stress and the activation of defense systems in different goldfish tissues