Effect of hypoxia tolerance on the relation between indicators of free radical oxidation of lipides and proteins in murine kidneys during the post-resuscitation period

Abstract

Aim. Study of the relationship between the parameters of free radical oxidation of proteins and lipids in the murine kidneys in the post-resuscitation period after stopping the systemic circulation, depending on their resistance to hypoxia. Methods. The systemic circulation was stopped by intra-thoracic clamping of the neurovascular bundle for 5 minutes, performed under general ether anesthesia in male noninbred white rats, divided after testing into two groups based on resistance to hypoxia. The observation period lasted for 35 days. In the homogenates of kidney tissues, the content of products reactive to tiobarbituric acid, carbonylated proteins, the formation of metal-catalyzed carbonylated proteins and bitirozin were determined. Results. The characteristic manifestation of oxidative stress in the recovery period after stopping blood circulation and resuscitation was found to be reciprocity of the relationship between the levels of lipoperoxidation and oxidative modification of proteins. Highly resistant to hypoxia animals were characterized by high resistance of proteins of kidney tissue to free radical oxidation against the background of high levels of lipid peroxidation. On the contrary, in animals non-resistant to hypoxia, against the background of relatively low values of lipoperoxidation, high levels of oxidative modification of proteins, both initial and induced, were recorded. Conclusion. In post-resuscitation period in highly resistant to hypoxia animals, marked activation of lipoperoxidation occurs accompanied by a transient increase in the carbonylation of proteins in the early observation period; for low-resistant to hypoxia animals high intensity of carbonyl stress against the background of the relative «preservation» of lipid structures of the cell is characteristic, which persists throughout the post-resuscitation period, which can make a significant contribution to kidney damage, increasing the risk of renal failure.