Background: Insecticide resistance inAnophelesmosquitoes is threatening the success of malaria control programmes. This is particularly true in Benin where pyrethroid resistance has been linked to the failure of insecticide treated bed nets. The role of mutations in the insecticide target sites in conferring resistance has been clearly established. In this study, the contribution of other potential resistance mechanisms was investigated inAnopheles gambiaes.s. from a number of localities in Southern Benin and Nigeria. The mosquitoes were sampled from a variety of breeding sites in a preliminary attempt to investigate the role of contamination of mosquito breeding sites in selecting for resistance in adult mosquitoes.Results: All mosquitoes sampled belonged to the M form ofAn. gambiaes.s. There were high levels of permethrin resistance in an agricultural area (Akron) and an urban area (Gbedjromede), low levels of resistance in mosquito samples from an oil contaminated site (Ojoo) and complete susceptibility in the rural Orogun location. The target site mutationkdrWwas detected at high levels in two of the populations (Akron f = 0.86 and Gbedjromede f = 0.84) but was not detected in Ojoo or Orogun. Microarray analysis using theAnopheles gambiaedetox chip identified two P450s,CYP6P3andCYP6M2up regulated in all three populations, the former was expressed at particularly high levels in the Akron (12.4-fold) and Ojoo (7.4-fold) populations compared to the susceptible population. Additional detoxification and redox genes were also over expressed in one or more populations including two cuticular pre-cursor genes which were elevated in two of the three resistant populations.Conclusion: Multiple resistance mechanisms incurred in the different breeding sites contribute to resistance to permethrin in Benin. The cytochrome P450 genes,CYP6P3andCYP6M2are upregulated in all three resistant populations analysed. Several additional potential resistance mechanisms were also identified that warrant further investigation. Metabolic genes were over expressed irrespective of the presence ofkdr, the latter resistance mechanism being absent in one resistant population. The discovery that mosquitoes collected from different types of breeding sites display differing profiles of metabolic genes at the adult stage may reflect the influence of a range of xenobiotics on selecting for resistance in mosquitoes.
Pharmaceutical industries are among the major contributors to industrial waste. Their effluents when wrongly handled and disposed of endanger both human and environmental health. In this study, we investigated the potential genotoxicity of a pharmaceutical effluent, by using the Allium cepa, mouse- sperm morphology, bone marrow chromosome aberration (CA) and micronucleus (MN) assays. Some of the physico-chemical properties of the effluent were also determined. The A. cepa and the animal assays were respectively carried out at concentrations of 0.5, 1, 2.5, 5 and 10%; and 1, 5, 10, 25 and 50% of the effluent. There was a statistically different (p < 0.05), concentration-dependent inhibition of onion root growth and mitotic index, and induction of chromosomal aberrations in the onion and mouse CA test. Assessment of sperm shape showed that the fraction of the sperm that was abnormal in shape was significantly (p < 0.05) greater than the negative control value. MN analysis showed a dose-dependent induction of micronucleated polychromatic erythrocytes across the treatment groups. These observations were provoked by the toxic and genotoxic constituents present in test samples. The tested pharmaceutical effluent is a potentially genotoxic agent and germ cell mutagen, and may induce adverse health effects in exposed individuals.
Environmental, plant and animal exposure to hazardous substances from electronic wastes (e-wastes) in Nigeria is increasing. In this study, the potential cytogenotoxicity of e-wastes leachate and contaminated well water samples obtained from Alaba International Electronic Market in Lagos, Nigeria, using induction of chromosome and root growth anomalies in Allium cepa, and micronucleus (MN) in peripheral erythrocytes of Clarias gariepinus, was evaluated. The possible cause of DNA damage via the assessments of liver malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH) and superoxide dismutase (SOD) as indicators of oxidative stress in mice was also investigated. There was significant (p < 0.05) inhibition of root growth and mitosis in A. cepa. Cytological aberrations such as spindle disturbance, C-mitosis and binucleated cells, and morphological alterations like tumor and twisting roots were also induced. There was concentration-dependent, significant (p < 0.05) induction of micronucleated erythrocytes and nuclear abnormalities such as blebbed nuclei and binucleated erythrocytes in C. gariepinus. A significant increase (p < 0.001) in CAT, GSH and MDA with concomitant decrease in SOD concentrations were observed in the treated mice. Pb, As, Cu, Cr, and Cd analyzed in the tested samples contributed significantly to these observations. This shows that the well water samples and leachate contained substances capable of inducing somatic mutation and oxidative stress in living cells; and this is of health importance in countries with risk of e-wastes exposure.
Information on the potentials of electronic waste (e-waste) leachate to induce genotoxicity in eukaryotic cells is scarce. In this study, we investigated the potential of raw and simulated e-waste leachates to induce cytotoxicity and DNA damage in Allium cepa. Roots of onion bulbs were grown in five concentrations: 1, 5, 10, 25 and 50% (v/v; leachate/tap water) of each of the leachate sample, tap water (negative control) and 0.25 ppm lead nitrate (positive control). Cytogenetic and root length inhibition analyses were evaluated at 48 and 72 hours respectively. There was concentration-dependent significant (p < 0.05) inhibition of root growth and cell proliferation compared to the negative control. The leachates also induced morphological modifications of the roots and cytological aberrations such as anaphase bridge, sticky chromosomes and binucleate cells. Fe, Cd, Mn, Cu, Ni, Cr As, Zn and Pb analysed in the samples were believed to play significant role in the observed cytogenotoxicity in A. cepa. These observations indicate that e-waste leachate contained substances capable of inducing cytotoxicity and somatic mutations in A. cepa. This is of environmental and public health importance in Nigeria and other developing nations whose populations are at risk of e-waste exposure.
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.
21 March 2011 in Toxicological & Environmental Chemistry
Human exposure to electronic waste (e-waste) is increasing, especially in developing nations. This has potential short and chronic adverse health risks. Information is currently scarce on potential genotoxicity of e-waste leachate. In this study, the potential mutagenic and genotoxic effects of leachates from e-waste dumpsites at two electronic markets in Lagos, Nigeria, were investigated. The assays utilized were: bone marrow micronucleus (MN) and chromosome aberration (CA), spermatogonia CA, sperm morphology, and sperm count in mice. Experiments were carried out at concentrations of 1%, 5%, 10%, 25%, and 50% (v/v; leachate: distilled water) of leachate samples. MN analysis showed a concentration-dependent induction of micronucleated polychromatic erythrocytes (MNPCE) across the treatment groups. In the CA tests (bone marrow and spermatogonia), there was concentration-dependent significant reduction in mitotic index and induction of different types of CA. Assessment of sperm shape showed a significant increase in sperm abnormalities with significant decrease in mean sperm count in treated groups. Heavy metals analyzed in the tested samples are believed to contribute significantly to the observed genetic damage. This indicates that e-waste contains potential genotoxic agents; and constitutes a genetic risk in exposed human population.