Abstract
Responses of wildlife to multiple stressors fit in the ecological concept of trade-off. While toxicity of non-steroidal anti-inflammatory drugs and heavy metals for free-ranging birds has been shown in single exposures, the present study aims to evaluate oxidative stress, and liver and kidney damage caused by single and combined effects of diclofenac and lead in the Japanese quail. Forty Japanese quail (Coturnix coturnix japonica) were divided into equal groups of controls, diclofenac, Pb, and Pb+diclofenac exposures. The birds were exposed to the respective chemicals through insertion of lead shots (1.5 g) into the crop on day 0 of the experiment and/or administration of 5 mg/kg of diclofenac intramuscularly in two treatments on days 0 and 5. Groups in liver and kidney tissues of birds were then compared after 10 days using histopathology and biochemistry markers such as glutathione reductase (GR), ferric reducing antioxidant power (FRAP), and lipid peroxidation measured as total thiobarbituric acid reactive species (TBARS). The liver damage score gradient was Pb+diclofenac exposure group > Pb exposure group > diclofenac exposure group and hepatic TBARS values were significantly increased in the group of birds exposed to a combination of diclofenac and lead compared to the healthy control group. The study has shown that, apart from the reported nephrotoxicity of diclofenac, hepatic toxicity should also be considered. Avian clinicians should be cautious when selecting drugs for therapy of wild birds with unknown history of exposure to toxic substances.
Highlights
Exposure of birds to multiple stressors elicits physiological costs and trade-off responses that may be represented by oxidative stress as a non-specific biochemical process (Constantini and Møller 2009).While sub-lethal adverse effects are underreported in ecotoxicology (Pikula et al 2010), various interactions, e.g. synergistic effects between natural stressors and environmental pollutants, are common (Fry 1995; Holmstrup et al 2010)
Groups in liver and kidney tissues of birds were compared after 10 days using histopathology and biochemistry markers such as glutathione reductase (GR), ferric reducing antioxidant power (FRAP), and lipid peroxidation measured as total thiobarbituric acid reactive species (TBARS)
The liver damage score gradient was Pb+diclofenac exposure group > Pb exposure group > diclofenac exposure group and hepatic TBARS values were significantly increased in the group of birds exposed to a combination of diclofenac and lead compared to the healthy control group
Summary
Exposure of birds to multiple stressors elicits physiological costs and trade-off responses that may be represented by oxidative stress as a non-specific biochemical process (Constantini and Møller 2009).While sub-lethal adverse effects are underreported in ecotoxicology (Pikula et al 2010), various interactions, e.g. synergistic effects between natural stressors and environmental pollutants, are common (Fry 1995; Holmstrup et al 2010). Findings in affected birds include residues of diclofenac, visceral gout and renal failure (Oaks et al 2004) Both wild and captive birds are at risk of lead toxicosis Despite high conservation concern this issue in terrestrial species such as raptors and upland game birds remains largely to be addressed (Fischer et al 2006) Species such as California condors were brought to the brink of extinction because of lead poisoning (Finkelstein et al 2012). Diclofenac has been shown to induce oxidative damage in liver (Islas-Flores et al 2013)
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