Abstract
Aim. To study the relation between the processes of mitochondrial oxidation and the intensity of lipid peroxidation, pulmonary and cardiac proteins oxidative modification at cranial injury, diabetes mellitus and at both. Methods. Experiments were carried out on 100 male white rats distributed to the following groups: the first group (n=10) - control group consisted of 10 intact animals, the second group (n=40) - rats with simulated cranial injury, the third group (n=10) - rats with experimental diabetes mellitus, the fourth group (n=40) - rats with simulated cranial injury and experimental diabetes mellitus. Experimental diabetes was induced by a single intraperitoneal injection of streptozotocin solution. Animals were withdrawn from the experiment at 3, 24 hours, 5 and 14 days after the cranial injury. Cardiac and pulmonary energy supply was estimated by the activity of succinate dehydrogenase, cytochrome oxidase and hydrogen potassium ATPase, as well as by the level of adenine nucleotides. Intensity of free-radical protein and lipid peroxidation was assessed by measuring the levels of neutral and base aldehyde and ketone derivatives and active products reacting with thiobarbituric acid. Results. Decrease of succinate dehydrogenase, cytochrome oxidase activity, a significant increase of hydrogen potassium ATPase activity in heart and lungs mitochondria was observed in rats with cranial injury, diabetes mellitus and especially with both conditions. Adenosine triphosphate tissue reserves have significantly decreased, while adenosine diphosphate and monophosphate levels increased, lipid peroxidation and protein oxidation processes activated. Conclusion. In rats with cranial injury associated with diabetes mellitus, lipid and protein peroxidation intensity parameters, the intensity of oxidative stress and the levels of macroergic substanses were significantly worse compared to the same parameters in the injured animals with normal blood glucose level.
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