Genotoxicity evaluation of Chlorfenapyr in exposed freshwater African catfish Clarias gariepinus using micronucleus test

Chlorfenapyr is a new formulated insecticide targeted against insecticide resistant species. Its application in targeting harmful aquatic insects may potentially contaminate aquatic environment. This study is to evaluate its genotoxic effects on non-targeted aquatic biota. The study assessed the genotoxic potentials of chlorfenapyr in African catfish (Clarias gariepinus) using the micronucleus (MN) test. Juvenile stage of C. gariepinus were exposed to different concentrations; 5.00 – 15.00 mgL-1 of chlorfenapyr for 96 hours, peripheral blood was collected through the caudal vein and examined for micronucleus induction in the erythrocytes. The tested concentrations of chlorfenapyr did not elicit significant [F (5, 18) = 0.167, p 0.971] increase in MN formation and other nuclear abnormalities in the peripheral erythrocytes of C. gariepinus. The outcome of this study gives credence to the view that chlorfenapyr is not clastogenic and or aneugenic to non-targeted aquatic vertebrate with reference to fish (C. gariepinus)

Liver and kidney dysfunction in wistar rats exposed to municipal landfill leachate. Res. Environ

Abstract There is limited information on the toxicity of landfill leachate on somatic tissues and organs of mammals. The hepatotoxic and nephrotoxic effects of leachates from Olusosun and Aba-Eku landfills in Southwestern Nigeria in Wistar albino rats were investigated. Rats orally exposed to 1 -25 % concentrations of each of the test leachates were examined for clinical signs of toxicity and body weight gain during exposure. Blood, liver and kidney of surviving rats were examined for serum biochemical parameters, organ weight gain and histopathology. Clinical toxicity signs include ungroomed hair, reduced activities, hair loss, laboured breathing, reduced feed and fluid consumption, abscess and muscular disorder. There was concentration dependent sex related significant (p<0.05) decrease in body weight and increase absolute and relative liver and kidney weight gain. The test samples caused increase in aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine but decrease albumin and total proteins. These parameters showed sexual dimorphisms. Histopathological lesions in the liver and kidney include mild to severe multifocal degeneration of the hepatocytes, multiple periportal foci, cellular infiltration, interstitial haemorrhage cortical congestion, degenerative epithelia of renal tubules and necrosis. The concentration of heavy metals and anions in the test samples were above standard permissible limits. These findings show the potentials of landfill leachate to induce liver and kidney dysfunction in rat probably via free radical formation and/or direct chemical disruption of the organs. This may be of health risk in animal and human population expose to chemical substances from waste landfills

Brain dysfunctions in Wistar rats exposed to municipal landfill leachates

Brain damage induced by Olusosun and Aba-Eku municipal landfill leachates was investigated in Wistar rats. Male rats were orally exposed to 1–25% concentrations of the leachates for 30 days. Catalase (CAT) and superoxide dismutase (SOD) activities, and malondialdehyde (MDA) concentrations in the brain and serum of rats were evaluated; body and brain weight gain and histopathology were examined. There was significant (p < 0.05) decrease in body weight gain and SOD activity but increase in absolute and relative brain weight gain, MDA concentration and CAT activity in both brain and serum of treated rats. The biochemical parameters, which were more altered in the brain than serum, corroborated the neurologic lesions; neurodegeneration of purkinje cells with loss of dendrites, perineural vacuolations of the neuronal cytoplasm (spongiosis) and neuronal necrosis in the brain. The concentrations of Cr, Cu, Pb, As, Cd, Mn, Ni, sulphates, ammonia, chloride and phosphate in the leachate samples were above standard permissible limits. The interactions of the neurotoxic constituents of the leachates induced the observed brain damage in the rats via oxidative damage. This suggests health risk in wildlife and human populations

Exposure To Effluent From Pharmaceutical Industry Induced Cytogenotoxicity, Hematological And Histopathological Alterations In Clarias Gariepinus (Burchell, 1822)

Pharmaceutical effluents contain toxic xenobiotics capable of contaminating aquatic environments. Untreated effluents are illegally discharged into aquatic environment in most developing countries. Pharmaceutical effluent induced alterations in biomarkers of genetic and systemic damage on rodents. However, information is relatively scarce on the possible cytogenotoxicity and systemic toxicity of this effluent on aquatic vertebrates. The study herein assessed the cytogenotoxic, hematological and histopathological alterations induced by pharmaceutical effluent in Clarias gariepinus. 96 h acute toxicity of the effluent was determined after C. gariepinus was exposed to six different concentrations (10 - 60 %) of the effluent. Subsequently, fish was exposed to sub-lethal concen-trations (2.18 - 17.41 %) obtained from the 96 h LC50 for 7 and 14 days after which micronucleus (MN) and nu-clear abnormalities (NAs) in peripheral erythrocytes were assessed as cytogenotoxic biomarkers, alterations in hematological indices and histopathological lesions were also examined. Fish, concurrently exposed to dechlo-rinated tap water and benzene (0.01 mL/L), served as negative and positive controls respectively. The derived 96 h LC50 of 17.41 % which was 1.89 times more toxic than the 24 h LC50 (32.95 %) showed that the effluent induced concentration-dependent mortality according to exposure duration. The effluent caused significant (p&lt;0.05) time-dependent increase in the frequency of MN and abnormal nuclear erythrocytes compared to the negative control. Also, there was decrease in total erythrocyte counts, hemoglobin and hematocrit concentrations and increase in leucocyte and lymphocyte counts. The effluent induced pathological lesions on gills, liver and kidneys of treated fish. Higher physicochemical parameters than standard permissible limits in the effluent are capable of inducing genomic instability and systemic damage in fish. Pharmaceutical effluent can increase micropollutants in aquatic environmental and health risks to aquatic biota. There is need to promulgate stringent laws against illegal discharge of effluents into aquatic environment

Experimental modeling of the acute toxicity and cytogenotoxic fate of composite mixtures of chromate, copper and arsenate oxides associated with CCA preservative using Clarias gariepinus (Burchell 1822)

Concurrent occurrence of chromium (Cr), copper (Cu) and arsenic (As) from chromated copper arsenate (CCA) wood preservative in aquatic ecosystems demands that their joint-actions in eliciting toxic effects be assessed for adequate understanding of the health risk they may pose to biota. Clarias gariepinus was exposed to As2O3 , CrO3 and CuO and their composite mixtures (1:1 and 1:1:1) at various concentrations (0 – 600 mg/L) for 96-h to determine the acute toxicity using OECD (1992) protocol. C. gariepinus was then exposed to sub-lethal concentrations corresponding to 6.25, 12.5, 25.0, 50.0 and 100% of the 96-h LC50 for 7 days to assess the cytogenotoxic effects using piscine micronucleus (MN) test. The 96-h LC50 showed that the metals/metalloid demonstrated differential interactions in a concentration dependent pattern. The 96-h LC50 showed that Cr was the most toxic while Cu and As:Cu were indeterminate (Cr &gt; Cr:Cu &gt; As:Cr &gt; As &gt; As:Cr:Cu &gt; Cu = As:Cu indeterminate). Isobologram and synergistic ratio (SR) models predicted antagonistic interaction between Cu:Cr and As:Cr and synergism between As:Cu in the causation of morbidity and mortality of C. gariepinus. Interaction factor model predicted antagonism as common interactive mechanism among the metal/metalloid mixtures in the induction of MN and abnormal nuclear erythrocytes in C. gariepinus. Predicted interactions among the three metals/ metalloid were largely antagonism and synergism towards the induction of acute toxicity and cytogenotoxicity. The models employed herein may be useful in establishing environmental safe limits for mixtures of metals/metalloids against the induction of acute toxicity and DNA damage in lower aquatic vertebrates

The genotoxicity and systemic toxicity of a pharmaceutical effluent in Wistar rats may involve oxidative stress induction

There is scarcity of information on the possible mechanisms of pharmaceutical effluent induced genotoxicity and systemic toxicity. This study investigated the genotoxicity and systemic toxicity of a pharmaceutical effluent in Wistar rats. Rats were orally treated with 5–50% concentrations of the effluent for 28 days. At post-exposure, blood, liver, kidney and bone marrow cells were examined for alterations in serum biochemical parameters and hematological indices, histopathological lesions and micronucleated polychromatic erythrocytes formation (MNPCE). The effluent caused concentration independent significant (p < 0.05) alterations in aspartate (AST) and alanine (ALT) aminotransferases, superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total and direct bilirubin and creatinine. There was reduction in red blood count (RBC), hemoglobin concentration (HGB), platelets, percentage hematocrit (HCT), white blood count (WBC) and mean corpuscle hemoglobin (MCH) except mean corpuscle hemoglobin concentration (MCHC), which increased in the treated rats. Histopathological lesions observed in the liver and kidney of the effluent treated rats were thinning of the hepatic cord, kuffer cell hyperplasia, vacuolation of the hepatocytes and renal cells, multifocal inflammatory changes, necrosis and congestion of the renal blood vessels and central vein. MNPCE significantly increase in the bone marrow of the treated rats compared to the negative control. The concentration of some toxic metals and anions in the effluent were above standard permissible limits. These findings showed that the pharmaceutical effluent caused somatic DNA damage and systemic toxicity in rats may involve induction of oxidative stress, suggesting environmental contamination and health risks in wildlife and humans

Exposure to effluent from pharmaceutical industry induced cytogenotoxicity, hematological and histopathological alterations in Clarias gariepinus (Burchell, 1822)

Pharmaceutical effluents contain toxic xenobiotics capable of contaminating aquatic environments. Untreated effluents are illegally discharged into aquatic environment in most developing countries. Pharmaceutical effluent induced alterations in biomarkers of genetic and systemic damage on rodents. However, information is relatively scarce on the possible cytogenotoxicity and systemic toxicity of this effluent on aquatic ertebrates. The study herein assessed the cytogenotoxic, hematological and histopathological alterations induced by pharmaceutical effluent in Clarias gariepinus. 96 h acute toxicity of the effluent was determined after C. gariepinus was exposed to six different concentrations (10 - 60 %) of the effluent. Subsequently, fish was exposed to sub-lethal concentrations (2.18 - 17.41 %) obtained from the 96 h LC50 for 7 and 14 days after which micronucleus (MN) and nuclear abnormalities (NAs) in peripheral erythrocytes were assessed as cytogenotoxic biomarkers, alterations in hematological indices and histopathological lesions were also examined. Fish, concurrently exposed to dechlorinated tap water and benzene (0.01 mL/L), served as negative and positive controls respectively. The derived 96 h LC50 of 17.41 % which was 1.89 times more toxic than the 24 h LC50 (32.95 %) showed that the effluent induced concentration-dependent mortality according to exposure duration. The effluent caused significant (p<0.05) time-dependent increase in the frequency of MN and abnormal nuclear erythrocytes compared to the negative control. Also, there was decrease in total erythrocyte counts, hemoglobin and hematocrit concentrations and increase in leucocyte and lymphocyte counts. The effluent induced pathological lesions on gills, liver and kidneys of treated fish. Higher physicochemical parameters than standard permissible limits in the effluent are capable of inducing genomic instability and systemic damage in fish. Pharmaceutical effluent can increase micropollutants in aquatic environmental and health risks to aquatic biota. There is need to promulgate stringent laws against illegal discharge of effluents into aquatic environment