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Shi, X.L., Jiang, H.G., Mao, Y., Ye, J.P. and Saffiotti, U. (1996) Vanadium (IV)-mediated free radical generation and related 2’-deoxyguanosine hydroxylation and DNA damage. Toxicology, 106, 27-38. doi:10.1016/0300-483X(95)03151-5

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• TITLE: Suppression of renal cell proliferation, induction of apoptosis and cell cycle arrest: Cytotoxicity of vanadium in broilers

  AUTHORS: Xiaodong Liu, Hengmin Cui, Xi Peng, Jing Fang, Wei Cui, Bangyuan Wu

  KEYWORDS: Dietary High Vanadium; Renal Cells; Apoptosis; Cell Cycle; Flow Cytometry (FCM); Broiler

  JOURNAL NAME: Health, Vol.4 No.2, February 27, 2012

  ABSTRACT: The aims of this study were to clarify the effects of high vanadium on the renal cell cycle and apoptosis in broilers. 420 one-day-old avian broilers were divided into six groups and fed on a control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. As tested by flow cytometry, the percentage of apoptotic renal cells was increased in high vanadium group II, III, IV and V when compared with that of control group. The Proliferating index (PI) of renal cell and the ratio of S, G2 + M phase cells were markedly decreased and population of G0/G1 cells was increased in high vanadium group II, III, IV and V. The results showed that dietary vanadium in excess of 15 mg/kg was toxic to kidney by the renal cells cycle arrest and increased apoptosis, which caused the growth depression of the kidney in broilers.