Literature DB >> 8126754

Effects of heat stress on Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of broiler chickens vital organs.

C L Chen1, S Sangiah, H Chen, J D Roder, Y Shen.   

Abstract

Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of brain, heart, kidney, and small and large intestinal mucosa of broiler chickens exposed to heat stress (41 degrees C, 65% relative humidity for 6 h) and thermoneutral (25 degrees C, 65% relative humidity) conditions were determined. Brain and kidneys were found to have significantly higher Na+,K(+)-ATPase activities than those of heart and intestinal mucosa. Mg(2+)-activated ATPase and Na(+)-ATPase activities in the intestinal mucosa were higher than those of brain, kidneys, and heart under thermoneutral conditions. While there was a significant inhibition of total ATPase, Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activity of small and large intestinal mucosa of broiler chickens exposed to heat stress, the inhibitory effect was limited to total ATPase and Na+,K(+)-ATPase enzymes in kidneys. Heat stress produced a significant increase only in Mg(2+)-activated ATPase activity of the heart, without a remarkable change in all forms of ATPase activity in the brain. Heat stress significantly decreased the ratio of Na+,K(+)-ATPase to Mg(2+)-ATPase in the heart, kidneys, and small and large intestinal mucosa. The percentage of Na(+)-ATPase in Na+,K(+)-ATPase of brain, heart, and kidneys did not significantly change during heat stress, but the ratio in small and large intestinal mucosa increased significantly during heat stress. The severe disturbances in both serum electrolytes and acid-base balance observed in previous heat stress studies could partly be mediated by direct or indirect effects of heat stress on Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of kidneys, and small and large intestinal mucosa of broiler chickens.

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Year:  1994        PMID: 8126754     DOI: 10.1080/15287399409531848

Source DB:  PubMed          Journal:  J Toxicol Environ Health        ISSN: 0098-4108


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