Abstract
Gyps species have been previously shown to be highly sensitive to the toxic effects of diclofenac, when present in their food sources as drug residues following use as a veterinary medicine. Vultures exposed to diclofenac soon become depressed and die with signs of severe visceral gout and renal damage on necropsy. The molecular mechanism behind toxicity and renal excretion of uric acid is still poorly understood. With the clinical pictures suggesting renal uric acid excretion as the target site for toxicity, as a first step the following study was undertaken to determine the uric acid excretory pathways present in the African white-backed vulture (Gyps africanus) (AWB), one of the species susceptible to toxicity. Using transcriptome analysis, immunohistochemistry and functional predictions, we demonstrated that AWB makes use of the organic anion transporter 2 (OAT2) for their uric acid excretion. RT-qPCR analysis subsequently demonstrated relatively similar expression of the OAT2 transporter in the vulture and chicken. Lastly docking analysis, predicted that the non-steroidal drugs induce their toxicity through an allosteric binding.
Highlights
Diclofenac related toxicity and mass die offs have been well documented for three Gyps species on the Asian continent following contamination of their food source from the veterinary use of the drug in cattle [1]
Further no chicken OAT3 partial sequence was present in the National Centre of Biotechnology Information (NCBI) database
In this study we conclude that AWB vulture kidney expresses OAT1 and organic anion transporter 2 (OAT2) mRNA but not OAT3
Summary
Diclofenac related toxicity and mass die offs have been well documented for three Gyps species on the Asian continent following contamination of their food source from the veterinary use of the drug in cattle [1]. Current speculation is that toxicity is linked to renal functionality as a result of pathological finding of visceral gout in recently dead birds. Gout is the pathological finding that results from the precipitation of urate salts into the abdominal cavity once the saturation point of plasma has been reached. As a substance uric acid is produced by the liver from the breakdown of purines both endogenous and exogenous, and maintained as a finely controlled suspension in the plasma [3].
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