Trivalent chromium induces oxidative stress in goldfish brain (original) (raw)
Related papers
Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, 2010
The present study directly compared the effects of exposure to Cr 6+ and Cr 3+ (10 mg/L) over 24, 48 and 96 h on indices of oxidative stress and activities of antioxidant and related enzymes in goldfish brain, liver, kidney and gills. Glutathione status clearly demonstrated the development of oxidative stress, whereas changes in protein carbonyls and lipid peroxides were less pronounced. The activity of superoxide dismutase (SOD) was virtually unaffected after 24 or 96 h exposure, but 48 h exposure to Cr 6+ reduced SOD activity in brain (by 30%), enhanced activity in kidney (by 28%) and had no effect on liver SOD. Chromium exposure for shorter times had no effect on catalase activity, whereas 96 h exposure depressed activity in liver, kidney and gills. Exposure to Cr 6+ reduced catalase activity in liver by 53% and in kidney by 21%, while in gills it was reduced by 20 and 38% by exposure to Cr 3+ and Cr 6+ , respectively. Exposure to chromium for 24 h did not affect glutathione-S-transferase activity, but treatment with Cr 6+ for 48 h enhanced it in brain by 1.5-fold, whereas exposure to Cr 3+ decreased activity by 29% in kidney. Fish treatment with chromium ions for 96 h decreased glutathione-S-transferase activity in liver by 51 and 25%, respectively. Chromium exposure had very little effect on the activities of GR or G6PDH. These data show that both chromium ions induced oxidative stress in goldfish tissues and affected the activity of antioxidant and associated enzymes.
Chromium(III) induces oxidative stress in goldfish liver and kidney
Aquatic Toxicology, 2009
In the environment chromium is found mainly in two valence states-hexavalent chromium (Cr 6+ ) and trivalent chromium (Cr 3+ ). The present study evaluates the effects of Cr 3+ exposure on goldfish by analyzing parameters of oxidative stress and antioxidant defense in liver and kidney of fish given 96 h exposures to Cr 3+ concentrations of 1, 2.5, 5 or 10 mg/l in aquarium water. Cr 3+ exposure did not alter two parameters of oxidative stress-protein carbonyl content and lipid peroxide concentrations in either organ. However, Cr 3+ 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 Cr 3+ exposure levels except in liver under the highest, 10 mg/l, exposure level. In liver, exposure to 1-5 mg/l Cr 3+ led to a decrease in the activity of superoxide dismutase (SOD) by 29-36%, and at 10 mg/l Cr 3+ the reduction was 54%, whereas in kidney ∼30% reductions in SOD activity were seen at concentrations 1 and 10 mg/l Cr 3+ . Catalase activity was not significantly affected by 1-5 mg/l Cr 3+ , 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 Cr 3+ effects on goldfish liver and kidney metabolism indicates that the trivalent ion induces stronger oxidative stress than Cr 6+ at the same concentrations.
Aquatic Toxicology, 2008
The effects of 96 h exposure to Cr 6+ (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 Cr 6+ 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 Cr 6+ . 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.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2010
Fish constitute an excellent model to understand the mechanistic aspects of metal toxicity vis-à-vis oxidative stress in aquatic ecosystems. Hexavalent chromium (Cr (VI)), due to its redox potential can induce oxidative stress (OS) in fish and impair their health. In the present investigation, we hypothesize that OS plays a key role in chromium induced toxicity in goldfish; leading to the production of reactive oxygen species (ROS) such as O • 2 , H 2 O 2 , OH • , and subsequent modulation of the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), metallothioneins (MT), glutathione proxidase (GPx), genotoxicity and histopathology. To test this hypothesis, antioxidant enzymes, DNA damage and histopathology assays were performed in liver and kidney tissues of goldfish exposed to different concentrations of Cr (VI) (LC 12.5 , LC 25 and LC 50) following 96h static renewal bioassay. The results of this study clearly show that the fish experienced OS as characterized by significant modulation of enzyme activities, induction of DNA damage and microscopic morphological changes in the liver and kidney. In both tissues, CAT activity was decreased whereas SOD activity and hydroperoxide levels were increased. In addition, GPx activity also increased significantly in higher test concentrations, especially in the kidney. MT induction and DNA damage were observed in both tissues in a concentration dependent manner. Microscopic examination of organ morphology indicated degeneration of liver tissue and necrosis of central vein. Necrosis of kidney tubular epithelial cells and tubules was observed at higher Cr (VI) concentrations. Taking together the findings of this study are helpful in organ-specific risk assessment of Cr (VI)-induced oxidative stress, genotoxicity and histopathology in fish.
Cytotoxicity of chromium ions may be connected with induction of oxidative stress
Chemosphere, 2010
Chromium ions are frequently found in aquatic ecosystems and are known to be inducers of oxidative stress in fish solid tissues. The present study was designed to determine whether fish blood samples can be used to allow nonlethal diagnostic testing for chromium intoxication. First, we confirmed that 96 h exposures to water containing 10.0 mg L À1 chromium ions, either Cr 3+ or Cr 6+ , induced oxidative stress in brain of goldfish (Carassius auratus). Multiple blood parameters were then evaluated. Cr 6+ exposure triggered a 579% increase in the number of erythrocytes containing micronuclei, a frequently used marker of cellular toxicity. Leucocyte numbers were also perturbed by exposure to either Cr 3+ or Cr 6+ indicating that chromium ions could impair the immune system as well. The content of protein carbonyl groups, a marker of oxidative damage to proteins, was enhanced in fish plasma by exposure to either chromium ion and activities of catalase and lactate dehydrogenase also were affected. The data demonstrate that chromium ions induced oxidative stress in goldfish blood and were cytotoxic for erythrocytes. This indicates that analysis of plasma can be used as a good early nonlethal diagnostic marker of fish intoxication by transition metal ions.
BioMed Research International, 2014
The evaluation of metal’s toxicity in freshwater is one of the imperative areas of research and there is an emergent concern on the development of techniques for detecting toxic effects in aquatic animals. Oxidative stress biomarkers are very useful in assessing the health of aquatic life and more in depth studies are necessary to establish an exact cause effect relationship. Therefore, to study the effectiveness of this approach, a laboratory study was conducted in the fishLabeo rohitaas a function of hexavalent chromium and the toxicity indices using a battery of oxidative stress biomarkers such as catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GR) in the liver, muscle, gills, and brain have been studied along with biometric parameters, behavioral changes, and Cr bioaccumulation. A significant increased HSI was observed in contrast to CF which reduced significantly. SOD, CAT, and GR activity increased significantly in all the tissues of treated fishes. The ...
Biomarker Insights, 2013
Chromium (Cr) is an abundant element in the Earth's crust. It exhibits various oxidation states, from divalent to hexavalent forms. Cr has diverse applications in various industrial processes and inadequate treatment of the industrial effluents leads to the contamination of the surrounding water resources. Hexavalent chromium (Cr (VI)) is the most toxic form, and its toxicity has been associated with oxidative stress. The present study was designed to investigate the toxic potential of Cr (VI) in fish. In this research, we investigated the role of oxidative stress in chromium-induced genotoxicity in the liver and kidney cells of goldfish, Carassius auratus. Goldfish were acclimatized to the laboratory conditions and exposed them to 5% and 10% of 96 hr-LC50 (85.7 mg/L) of aqueous Cr (VI) in a continuous flow through system. Fish were sampled every 7 days for a period of 28 days to analyze the lipid hydroperoxides (LHP) levels and genotoxic potentials in the liver and kidney. LHP ...
Study on Effects of Chromium on Antioxidant Enzymes in Mice
International Research Journal of Pharmacy, 2019
Chromium, naturally occurring, largest environmental toxicant that affects human health and most common pollutant; over the last few decades, it has been a concern that the fresh water consisting of massive metals can be agitated because of their campaigns primarily through the fraudulent programs of humans, industrial and domestic programs, chromium, heavy metal, primarily in oxidation states of hexavalent. Chromium obstructs the metabolic pathways and despite of all the above Chromium is an essential nutrient. Chromium adverse effects at low level is not well established. Hence, the study intended to examine the alterations of chronic exposure to chromium at low dose on antioxidant defense enzymes in mice. Exposure to chromium depleted significantly in catalyses, superoxide dismutase, and GST activity (p < 0.0001) in brain, liver and kidney when compared with their respective control group. The catalyses are considered one of the most important free radical scavenging enzymes, and the body's secondary protection against oxygen metabolites produced by the transformational massive metals increased activity levels of CAT, GST and SOD formation was observed experimental animals. The increase in antioxidant enzymes in Cr-treated animals indicated that one of the Cr-induced toxic effects as generated free radicals and in turn damages cell membrane.
Fish, being an important native of the aquatic ecosystem, are exposed to multipollution states and are therefore considered as model organisms for ecotoxicological studies of aquatic pollutants, including metal toxicity. We investigated oxidative stress (OS) in liver, kidney and gill tissues through antioxidant enzyme activities and genotoxicity induced in whole blood and gill tissues through comet assay and micronucleus (MN) test in Cyprinus carpio after 96-hour in vivo static exposure to potassium dichromate at three sublethal (SL) test concentrations, including SL-I [93.95 mg/L, i.e. one quarter of half-maximal lethal concentration (LC50)], SL-II (187.9 mg/L, i.e. one half of LC50), and SL-III (281.85 mg/L, i.e. three quarters of LC50), along with a control. The 96-hour LC50 value for potassium dichromate was estimated to be 375.8 mg/L in a static system in the test species. Tissues samples were collected at 24, 48, 72 and 96 hours postexposure. Results indicated that the exposed fish experienced OS as characterized by significant (p50.05) variation in antioxidant enzyme activities, as compared to the control. Activities of superoxide dismutase and glutathione peroxidase increased, whereas activity of catalase decreased with the progression of the experiment. The mean percent DNA damage in comet tail and MN induction in gills and whole blood showed a concentration-dependent increase up to 96-hour exposure. The findings of this study would be helpful in organ-specific risk assessment of Cr(VI)-induced OS and genotoxicity in fishes.
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 2012
Flatfish species, such as the turbot (Scophthalmus maximus), are common targets for toxic effects, since they are exposed through the food chain (ingestion of contaminated preys) and are in direct contact with the waterborne contaminant and sediments. Furthermore, these fish species live in close proximity to interstitial water that frequently dissolves high amounts of contaminants, including metals. Despite this significant set of characteristics, the present knowledge concerning flatfish contamination and toxicity by metals is still scarce. To attain the objective of assessing the effects of metals on a flatfish species, S. maximus specimens were chronically exposed to lead, copper and zinc, at ecologically relevant concentrations, and biochemical (oxidative stress: catalase and glutathione S-transferases activities, and lipid peroxidation; neurotoxicity: cholinesterase activity) parameters were assessed on selected tissues (gills and liver). Copper had no significant effects on all tested parameters; lead was causative of significant increases in liver GSTs activities and also in lipoperoxidation of gill tissue; exposure to zinc caused a significant increase in catalase activity of gill tissue. None of the tested metals elicited noteworthy effects in terms of neurotoxicity. The obtained results showed that only the metal lead is of some environmental importance, since it was able to cause deleterious modifications of oxidative nature at relevant concentrations.