ABSTRACT
A shift of breaking point to higher temperatures was illustrated on Arrhenius plots in kidney, liver and heart mitochondria of heat-adapted rats on 4.1, 2.7, 2.4 degrees C respectively. Q10 mitochondrion respiration fall in adapted animals in a range of 26-36 degrees C was indicative of temperature compensation. It was shown the elevation of phospholipid plasmalogen form content in heart and kidney mitochondria; as well as saturated fatty acids content in liver mitochondria. Structure and function changes were suggested to be the basic point of elevation of mitochondrion functional ability at high ambient temperature.
Subject(s)
Adaptation, Physiological/physiology , Hot Temperature , Mitochondria/physiology , Oxygen Consumption/physiology , Phospholipids/physiology , Temperature , Animals , Atmosphere Exposure Chambers , Fatty Acids/analysis , Fatty Acids/physiology , Kidney/analysis , Kidney/physiology , Mitochondria/analysis , Mitochondria, Heart/analysis , Mitochondria, Heart/physiology , Mitochondria, Liver/analysis , Mitochondria, Liver/physiology , Phospholipids/analysis , RatsABSTRACT
A study was made of the content of phospholipids, cerebrosides and cerebroside sulfates in the central nervous system of mice with experimental acute viral encephalomyelitis. No considerable changes in phospholipid content were revealed. A significant drop in the content of cerebrosides and cerebroside sulfates was defected in the CNS, being more pronounced in the spinal cord of sick animals. The reduction in the content of glycolipids can be explained by myelin disintegration and by the effect of viruses on the olygodendrocytes in which cerebrosides and cerebroside sulfates are synthesized.