Tag Archives: rhabdomyolysis

Labile iron pool formation in rat’s blood under rhabdomyolysis

S. G. Shandrenko

Palladin Institute of Biochemistry, National Academy of Siences of Ukraine, Kyiv;
e-mail: shangr-s@yandex.ru

The labile nonheme iron pool formation in blood under glycerol induced rhabdomyolysis in rats has been investigated. This iron is not included in transferrin, thereby it is redox-active. Rhabdomyolysis was caused by intramuscular injection of 50% glycerol in a dose of 10 ml/kg. In the first day it has been registered that the blood plasma free heme content increased 10 times and the liver heme-oxigenase activity increased 6 times. Plasma redox-active iron pool formation has been registered by EPR method. Such iron was absent in the control group. This iron pool content in the interval from the 1st to the 6st day was more than 2 mg/l and significantly higher than the transferrin iron level. The plasma iron pool unshielded by transferrin may be one of oxidative stress causes.

Carbohydrate and nitrogenous metabolism condition in the rat tissue under experimental rhabdomyolysis

P. A. Kaliman, S. M. Okhrimenko

Karazin Kharkiv National University, Ukraine;
e-mail: s.okhrimenko@mail.ru

Some effects of glycerol injection on indices of the condition of the thiol-disulfide system as well as carbohydrate and nitrogen metabolism in rats in vivo were studied. A decrease was revealed in levels of non-protein SH-groups in the liver, kidney and heart, as well as of protein SH-groups in the kidney and heart of rats following glycerol injection. That might be connected with SH-group oxidation under the excessive arrival of free haem into tissues under rhabdomyolysis. A decrease in glycogen and  increase in tyrosine aminotransferase activity in the liver were observed. Activation of nitrogenous metabolism following glycerol injection is indicated by the increase of aminotransferase activity in organs, and concentration of blood urea. High concentration of creatinine in the rat serum can reflect malfiltration in kidneys.

Amine oxidases as important agents of pathological processes of rhabdomyolysis in rats

O. O. Gudkova, N. V. Latyshko, S. G. Shandrenko

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
e-mail: ogudkova@biochem.kiev.ua

In this study we have tested an idea on the important role of amine oxidases (semicarbazide-sensitive amine oxidase, diamine oxidase, polyamine oxidase) as an additional source of oxidative/carbonyl stress under glycerol-induced rhabdomyolysis, since the enhanced formation of reactive oxygen species and reactive carbonyl species in a variety of tissues is linked to various diseases. In our experiments we used the sensitive fluorescent method devised for estimation of amine oxidases activity in the rat kidney and thymus as targeted organs under rhabdomyolysis. We have found in vivo the multiple rises in activity of semicarbazide-sensitive amine oxidase, diamine oxidase, polyamine oxidase (2-4.5 times) in the corresponding cell fractions, whole cells or their lysates at the 3-6th day after glycerol injection. Aberrant antioxidant activities depended on rhabdomyolysis stage and had organ specificity. Additional treatment of animals with metal chelator ‘Unithiol’ adjusted only the activity of antioxidant enzymes but not amine oxidases in both organs. Furthermore the in vitro experiment showed that Fenton reaction (hydrogen peroxide in the presence of iron) products alone had no effect on semicarbazide-sensitive amine oxidase activity in rat liver cell fraction whereas supplementation with methylglyoxal resulted in its significant 2.5-fold enhancement. Combined action of the both agents had additive effect on semicarbazide-sensitive amine oxidase activity. We can assume that biogenic amine and polyamine catabolism by amine oxidases is upregulated by oxidative and carbonyl stress factors directly under rhabdomyolysis progression, and the increase in catabolic products concentration contributes to tissue damage in glycerol-induced acute renal failure and apoptosis stimulation in thymus.