AJP - Endocrinology and Metabolism, Vol 267, Issue 1 E57-E62, Copyright © 1994 by American Physiological Society
Melatonin prevents the suppression of cardiac Ca(2+)-stimulated ATPase activity induced by alloxan
L. D. Chen, P. Kumar, R. J. Reiter, D. X. Tan, L. C. Manchester, J. P. Chambers, B. Poeggeler and S. Saarela
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio 78284-7762.
The effects of melatonin treatment on cardiac sarcolemmal membrane function
were investigated in alloxan-injected rats. Ca(2+)-stimulated
adenosine-triphosphatase (ATPase, Ca2+ pump) and Mg(2+)-ATPase activities
were depressed significantly in sarcolemmal preparations from
alloxan-injected rats compared with levels in control rats. These deficits
were observed 2 days after alloxan injection, and they were accompanied by
an increase in the density of voltage-sensitive calcium channels, as
measured by the [3H]nitrendipine-binding assay. In a dose-dependent manner,
treatment of rats with melatonin before alloxan injection significantly
overcame the suppression of Ca(2+)-stimulated ATPase in cardiac sarcolemma.
Melatonin (1, 5, and 10 mg/kg) overcame Ca(2+)-stimulated ATPase
suppression by 13, 35, and 70%, respectively. In addition, melatonin at a
dose of 10 mg/kg also prevented the suppression of the Mg(2+)-ATPase by
31%. The number of [3H]nitrendipine-binding sites was not influenced by
melatonin. The patent Na(+)-K(+)-ATPase and ouabain-sensitive
Na(+)-K(+)-ATPase activities were not different between the control and
experimental groups. The results indicate that Ca2+ pump activity is
suppressed by acute alloxan treatment, whereas the density of
voltage-sensitive calcium channels is increased. These changes may be a
consequence of alloxan toxicity to the cardiac sarcolemma. Melatonin,
likely because of its antioxidant capacity, exerts a protective effect on
heart sarcolemmal membrane function in alloxan-injected rats.
