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Hormones and liver mitochondria: effects of growth hormone and thyroxine on respiration, fluorescence of 1-anilino-8-naphthalene sulfonate and enzyme activities of complex I and II of submitochondrial particles
Authors:V T Maddaiah  S Clejan  A G Palekar  P J Collipp
Institution:Department of Pediatrics, Nassau County Medical Center and Stony Brook Health Sciences Center, State University of New York, East Meadow, New York 11554 USA
Abstract:The effects of hypophysectomy and subsequent administration of bovine growth hormone (0.1 IU/100 g body wt) and l-thyroxine (5 μg/100 g body wt) on respiration, energization-dependent fluorescence of 1-anilino-8-naphthalene sulfonate, NADH dehydrogenase, energy-independent nicotinamide nucleotide transhydrogenase, and succinate dehydrogenase activities were investigated in submitochondrial particles of rat liver. Hormones were injected daily for 7 days. Hypophysectomy decreased the respiratory rate with NADH or succinate and the activities of the three enzymes. Administration of growth hormone increased the respiration but showed selectivity toward NADH. Thyroxine increased the respiration more than growth hormone did with both substrates. Growth hormone increased the activities of NADH dehydrogenase and transhydrogenase whereas thyroxine increased the activity of only succinate dehydrogenase. After growth hormone treatment transhydrogenase activity was increased to about three times that of controls which may have significance in some processes mediated either directly or permissively by growth hormone. When both hormones were injected together, there was a significant decrease in the thyroxine-dependent rise in respiration on succinate as well as the growth hormone-dependent rise in enzyme activities. Fluorescence yield of 1-anilino-8-naphthalene sulfonate in unenergized submitochondrial particles remained unchanged independent of the hormonal status. Energization with succinate or NADH increased the fluorescence yield by about 2–20 times. Several parameters of energizationdependent fluorescence were decreased after hypophysectomy. In restoring these parameters, growth hormone and thyroxine showed specificity toward the energization substrate NADH and succinate, respectively. From the present results we conclude that (a) growth hormone and thyroxine regulate mitochondrial activity by affecting different segments of the respiratory chain, namely Complex I and Complex II, respectively, and (b) growth hormone and thyroxine exert moderating effects on one another.
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