Biomedical subjects

K Shivakumar

Publications and source records attributed to K Shivakumar.

21 records · Page 2Linked to original sources

PubMed1986

Salinity adaptation in fish: interaction of thyroxine with fish gill mitochondria.

When the freshwater fish Sarotherodon mossambicus is exposed to an ionoosmotic stress, extensive changes take place in the energetics of the gill mitochondria. These changes are reversed when thyroxine is administered to the fish prior to exposure to stress [K. Shivakumar and J. Jayaraman (1984) Arch. Biochem. Biophys. 233, 728]. The presence of a thyroxine binding component in the mitochondrial inner membrane, its characteristics, and its possible involvement in the salinity adaptation process are discussed.

Adaptation, Physiological↗

PubMed1984

Salinity adaptation in fish: effect of thyroxine on mitochondrial status.

Upon transfer of the fresh-water fish, Sarotherodon mossambicus, to 50% sea water, extensive changes take place in the functions of the gill mitochondria. The changes are (i) loss of ADP/O and RCI; (ii) loss of the ability to contract upon addition of ATP-Mg2+; (iii) lowered energy-dependent 45Ca uptake; (iv) increased amino acid incorporation capacity; (v) increased adenine nucleotide content; and (vi) a higher endogenous Ca2+ content. Administration of thyroxine to the fish reversed these changes, and the effect of thyroxine was also not transient. It is suggested that thyroxine promotes mitochondriogenesis, thereby effecting a restoration of the stress-affected mitochondrial functions.

Adaptation, Physiological↗

PubMedDate not supplied

Depressed antioxidant defense in rat heart in experimental magnesium deficiency. Implications for the pathogenesis of myocardial lesions.

Magnesium (Mg) deficiency has been shown to produce myocardial lesions in different experimental models. Based on several lines of evidence, it has been proposed that oxidative injury to the cardiac muscle may explain the pathobiology of such lesions. In pursuance of this postulation, the present study examined the effect of dietary deficiency of Mg on the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase, in rat heart. This article reports a significant lowering of the activity of both these enzymes in the cardiac tissue in Mg-deficient rats. Since depressed antioxidant defense in the heart may enhance myocardial susceptibility to oxidative injury, the observation is of possible relevance to the pathogenesis of cardiac lesions in Mg deficiency.

Animals↗