Carbofuran and its toxic metabolites provide forensic evidence for furadan exposure in vultures (Gyps africanus) in Kenya.

Department of Chemistry, Maseno University, P.O. Box 333, 40105 Maseno, Kenya.
Bulletin of Environmental Contamination and Toxicology (Impact Factor: 1.11). 04/2010; 84(5):536-44. DOI: 10.1007/s00128-010-9956-5
Source: PubMed

ABSTRACT Forensic analysis of carbofuran residues in weathered tissue samples for evidence of Furadan exposure in vultures (Gps africanus) by HPLC gave concentration (mg/Kg dry tissue weight) ranges of bdl - 0.07 (carbofuran), bdl - 0.499 (3-ketocarbofuran) and 0.013-0.147 (3-hydroxycarbofuran) in beaks, bdl-0.65 (carbofuran), 0.024-0.190 (3-ketocarbofuran) and 0.017-0.098 (3-hydroxycarbofuran) in feet, 0.179-0.219 (3-ketocarbofuran) and 0.081-0.093 (3-hydroxycarbofuran) in crop content, 0.078-0.082 (3-ketocarbofuran) and 0.091-0.101 (3-hydroxycarbofuran) in muscle of a laced carcass and 0.006-0.014 (carbofuran), 0.590-1.010 (3-ketocarbofuran) and 0.095-0.135 (3-hydroxycarbofuran) in soil sampled from a poisoning site. These compounds were confirmed by GC-MS. The results showed that HPLC combined with GC-MS is suitable for forensic analysis of carbofuran residues in bird tissue samples and that forensic investigation should include its two toxic metabolites, 3-hydroxycarbofuran and 3-ketocarbofuran.

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    ABSTRACT: The present work aimed to evaluate the toxic effects of two sublethal concentrations of carbofuran pesticide (0.16 and 0.49mg/L, for 35 days) on hematological and blood biochemical parameters of catfish, Clarias gariepinus, and to evaluate the genotoxic potential of carbofuran on the erythrocytes of C. gariepinus for the first time by micronucleus and erythrocyte alteration assays. The results revealed a significant (p<0.05) decrease in red blood cells (RBCs) count, haemoglobin (Hb) concentration, haematocrit (Hct) and the mean corpuscular haemoglobin concentration (MCHC) levels, but the mean corpuscular volume (MCV) and the mean corpuscular haemoglobin (MCH) levels were increased. White blood cells (WBCs) count, neutrophils, eosinophils, basophils and monocytes were increased significantly (p<0.05), while the lymphocytes were decreased. Also, carbofuran exposure caused a significant (p<0.05) increase in aspartic aminotransferase (AST) and alanine aminotransferase (ALT) and a significant (p<0.05) decrease in alkaline phosphatase (ALP) activity. The results obtained showed a significant (p<0.05) increase in plasma glucose, total lipids, urea and creatinin levels, but the total protein, albumin concentration and globulin levels were decreased (p<0.05) significantly and consequently A/G ratio also decreased. Carbofuran caused many genotoxic and morphological alterations in erythrocytes such as formation of micronuclei (MN), echinocytes, acanthocytes, tear like drop cells, microcytes and erythrocytes with vacuolated cytoplasm and pale nucleus. The exposed groups have shown significant variations in frequencies of MN and altered erythrocytes in comparison to control group, and these frequencies increased significantly (p<0.05) with the increase of carbofuran concentration. Therefore, current results present a clear evidence of the response of C. gariepinus to carbofuran and allow us to consider that C. gariepinus as a good bioindicator to reflect the toxicity and the genotoxic potential of carbofuran that might be released into the aquatic ecosystems.
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    ABSTRACT: Poisons have long been used to kill wildlife throughout the world. An evolution has occurred from the use of plant- and animal-based toxins to synthetic pesticides to kill wildlife, a method that is silent, cheap, easy, and effective. The use of pesticides to poison wildlife began in southern Africa, and predator populations were widely targeted and eliminated. A steep increase has recently been observed in the intensity of wildlife poisonings, with corresponding population declines. However, the majority of poisonings go unreported. Under national laws, it is illegal to hunt wildlife using poisons in 83% of African countries. Pesticide regulations are inadequate, and enforcement of existing legislation is poor. Few countries have forensic field protocols, and most lack storage and testing facilities. Methods used to poison wildlife include baiting carcasses, soaking grains in pesticide solution, mixing pesticides to form salt licks, and tainting waterholes. Carbofuran is the most widely abused pesticide in Africa. Common reasons for poisoning are control of damage-causing animals, harvesting fish and bushmeat, harvesting animals for traditional medicine, poaching for wildlife products, and killing wildlife sentinels (e.g., vultures because their aerial circling alerts authorities to poachers’ activities). Populations of scavengers, particularly vultures, have been decimated by poisoning. Recommendations include banning pesticides, improving pesticide regulations and controlling distribution, better enforcement and stiffer penalties for offenders, increasing international support and awareness, and developing regional pesticide centers.
    Annals of the New York Academy of Sciences 04/2014; · 4.38 Impact Factor
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    ABSTRACT: The present study examined the impacts of carbofuran on endocrinology of the catfish, Clarias gariepinus, for the first time and evaluated cortisol (CRT), triiodothyronine (T3), thyroxin (T4), 17β-estradiol (E2) and testosterone (TST) and the oxidative stress markers including SOD, CAT, GSTs, GSH. The toxic effects on the metabolic enzymes, G6PDH and LDH, in addition to lipid peroxidation (LPO) and DNA damage as biomarkers in Nile catfish, to sublethal exposures of carbofuran (0.16 and 0.49mg/L, for 35 days) were studied. Statistically significant differences between selected parameters between control and carbofuran-treated fish were recorded. Carbofuran caused a significant (p<0.05) increase in CRT and T3 levels; the mean levels of T4, TST, E2 exhibited significant decreases (p<0.05) in carbofuran-treated fish. Toxicity of carbofuran on liver, kidney, gills, gonads and muscles after 35 days of exposure was found. Glycogen levels showed a highly significant decrease in liver and gills (p< 0.001), a significant decrease (p< 0.05) in kidney and muscles, and insignificant changes (p>0.05) in gonads of treated fish. The two metabolic enzymes G6PDH and LDH in all tissues exhibited significant decreases (p<0.05) in treated fish. SOD, CAT, GSH and GST levels showed significant decreases (p<0.05) in all tissues of fish after exposure to carbofuran. LPO levels increased significantly (p<0.05) in all tissues except gonads after 5 weeks of exposure to carbofuran. There was a significant (p<0.05) increase in DNA fragmentation percentage in treated fish. Our results provide a clear evidence on the response of C. gariepinus to sublethal doses of carbofuran and allow us to consider catfish as a good bioindicator to reflect the endocrine disrupting impacts of carbofuran, and reflect the potential of this pesticide to cause disturbance in antioxidant defense system as well as metabolism and induction of lipid peroxidation (LPO) and DNA damage in contaminated ecosystems.
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Peter Otieno