Lipid peroxidation parameters in the internal organs of rats with different degrees of resistance to hypoxia

Lipid peroxidation and the antioxidant system of the heart, liver, and brain are studied in adult male Wistar rats with high and low resistance to hypoxia tested by “raising” to an altitude of 11.5 km and in intact outbred rats. These parameters are found to be the same in the brain of low- and high-resistance rats, while the brain content of lipid peroxidation products is higher in both groups of Wistar rats compared with outbred rats. The heart and liver parameters are coupled to the resistance to hypoxia. Antioxidant activity prevails over lipid peroxidation in the hearts and livers of high-resistance rats, confirming that oxidation plays a major role in the damaging and lethal effects of acute hypoxia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 1, pp 26–29, January, 1996 Presented by A. I. Archakov, Member of the Russian Academy of Medical Sciences     

Antenatal effects of ethanol and limontar on lipid peroxidation and the antioxidant defense system in the brain and liver of rat progeny

In contrast to short-term exposure, prolonged exposure to ethanol in the anternatal period is found to inhibit lipid peroxidation in the brain and liver of rats. Activation of the system of antioxidant defense in the brain and liver is observed after both short-and long-term exposure to ethanol. After short-term ethanol exposure, limontar normalizes lipid peroxidation. Translated fromByulleten' Eksperimental'noii Biologii i Meditsiny, Vol. 117, N ^o 1, pp. 41–44, January, 1994 Presented by M. Ya. Studenikin, Member of the Russian Academy of Medical Sciences     

Effect of the season on lipid peroxidation in the myocardium of rats with different resistance to hypoxia

Lipid peroxidation and the antioxidant system of the myocardium of adult male Wistar rats with low and high resistance to acute hypoxia tested by “raising” to an altitude of 11.5 km are studied in winter and in summer. It is found that the winter season is a mild stressor inducing changes in the myocardial antioxidant system and lipid peroxidation which are similar to those observed at the early stages of catecholamine stress in the summer season. In both cases alterations are more pronounced in low-resistance than in high-resistance rats. In winter, in low-resistance rats the intensity of lipid peroxidation and the activity of the antioxidant system are lower, while the ratio of their parameters (chemiluminescence data) is higher. At the same time, the levels of thiobarbituric acid-reactive substances are higher in winter in both groups. The relationship between the studied parameters and the resistance of rats to hypoxia is more obvious in winter than in summer, i.e., it is season-dependent and is also more pronounced in catecholamine stress. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N^olo 7, pp. 87–90, July, 1995 Presented by N. A. Agadzhanyan, Member of the Russian Academy of Medical Sciences     

Effect of ozone on lipid peroxidation in rat hearts isolated against the background of clinical death

Clinical death of outbred albino rats ensues after rapid blood loss due to a cut in the coronary coronary artery. Five minutes later, the isolated heart is perfused with ozonized Krebs-Henseleit solution. The activity of the antioxidant system in the heart is increased compared with that during routine oxygenation. The intensity of lipid peroxidation assessed by the intensity of chemiluminescence and the amount of lipid peroxidation products is significantly decreased during ozonization. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, № 2, pp. 161–163, February, 1996 Presented by B. A. Korolev, Member of the Russian Academy of Medical sciences     

Adaptation to periodic hypoxia and a diet supplemented with polyunsaturated class ω-3 fatty acids enhance the resistance of Ca2+ transport in the myocardial sarcoplasmic reticulum to free-radical oxidation

The relationship between the level of accumulation of lipid peroxidation products and the status of the Ca²⁺-transporting system in the sarcoplasmic reticulum of the rat myocardium is studied against the background of two cardioprotective factors, namely adaptation to periodic hypoxia and a diet enriched in polyunsaturated fatty acids of the ω-3 class. It is shown that the diet leads to an increase of level of lipid peroxidation products by 1.8 times in the heart and by 19 times in the liver, whereas a adaptation has no effect on the level of lipid peroxidation products in either of these organs. At the same time, the combined action of both factors considerably enhances the resistance of the myocardial Ca²⁺-transporting system to free radical-induced oxidation. Inin vitro experiments it is shown that adaptation to periodic hypoxia results in a more than twofold deceleration of Ca²⁺ transport inhibition during the oxidation induction by the Fe²⁺/ascorbate system; the diet causes a 3.5-fold deceleration of such inhibition. The results show that the accumulation of a high level of lipid peroxidation products is not always followed by damage to the Ca²⁺-transporting system in the myocardial sarcoplasmic reticulum. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N ^o 7, pp. 42–45, July, 1995 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Effects of adaptation to hypoxia on cytochrome levels in the brain and liver of rats

After a prolonged (for 30 days) adaptation of rats to intermittent hypoxia, their brains contained lowered levels of mitochondrial cytochromes, despite an increase in the number of mitochondria in the brain tissue mass, along with similar levels of high-energy compounds and more protein as compaired to the brains of unadapted controls. A mitochondrial population with novel properties presumably emerged in the brain. These effects were all more strongly marked in rats with an initially low resistance to hypoxia. In the liver of hypoxiaadapted animals, unlike in their brain, cytochrome levels in the mitochondrial and microsomal redox chains were lowered and the biogenesis of mitochondria was much less intensive. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N ^o 12, pp. 576–579, December, 1995     

The use of a nonopiate leu-enkephalin analog and of hydra peptide morphogen for the correction of proliferation disturbances in tracheal epithelium and of LPO processes in lungs of newborn rats exposed to prenatal hypoxia

Newborn rats were born of females exposed to high-altitude hypoxia. Pregnant females were injected i.p. either nonopiate leu-enkephalin analog or hydra peptide morphogen 10 μg/kg 30 min prior to being placed in a pressure chamber. Prenatal hypoxia causes the inhibition of the proliferative processes in tracheal epithelium and activation of lipid peroxidation (LPO) in lungs of newborn rats. The administration of nonopiate leu-enkephalin analog prevents the development of posthypoxic alterations in newborn rats. The administration of hydra peptide morphogen inhibits the proliferation of tracheal epithelium and lowers the activity of the antioxidant defense of the lungs in newborn rats. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N ^o 5, pp. 535–537, May, 1994 Presented by Yu. A. Romanov, Member of the Russian Academy of Medical Sciences     

Changes in the serum antioxidant system and lipid peroxidation under the influence of asbestos

The iron content, the state of the serum antioxidant system, and their relationship with the changes in lipid peroxidation in rat liver and lungs at the early stages of chrysotile-asbestos action, and the effect of the naturally occurring flavonoid rutin are studied. Intensification of lipid peroxidation in the liver and lungs and an increase in the oxyproline content, which correlates with the rise in serum antioxidant activity, are observed four weeks after a single intratracheal administration of 50 mg asbestos. The total serum iron content remains unchanged. Rutin has a pronounced anti-asbestos effect, inhibits the early stages of fibrosis, and facilitates normalization of the antioxidant system imbalance induced by asbestos. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 8 pp. 145–147, August, 1994     

Effects of adaptation to periodic hypoxia on kinetic parameters of respiratory chain enzymes in rat brain

A study of kinetic parameters of brain respiratory enzymes revealed that the maximal velocity and the Michaelis apparent constant for NADH-cytochrome C-reductase are significantly lower in low-resistant rats than in rats with a high resistance to hypoxia. Adaptation to periodic hypoxia increases total resistance only in low-resistant rats. It is accompanied by an increase in the values of kinetics parameters for NADH-cytochrome C-reductase and cytochrome oxidase. Kinetic parameters for these enzymes in the brain of high-resistant rats are either unaltered or even decreased. It is suggested that the first enzymatic complex of the respiratory chain is one of the limiting or regulating links in energy metabolism determining the brain's resistance to hypoxia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 3, pp. 252–255, March, 1996.     

Protective effects of trimetazidine in acute hypoxia

Trimetazidine improves resistance to acute hypobaric hypoxia. Intraperitoneal injection of this preparation in an optimal protective dose (25 mg/kg) to rats prevents serious disturbances of energy metabolism and activation of lipid peroxidation in the brain, heart, and liver. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 125, No. 4, pp. 410–412, April, 1998     

Adaptation to altitude hypoxia limits lipid peroxidation during inflammation and stress

Preadaptation of rats to altitude hypoxia results in reduced activation of lipid peroxidation during subsequent stress, inflammation, or both, as compared to hypoxiaunadapted animals, with the result that secondary changes in organs and tissues of adapted rats are much less pronounced and conditions are created for alleviating the acute inflammation and the stress reaction. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 6, pp. 590–593, June, 1995 Presented by E. D. Gol'dberg, Member of the Russian Academy of Medical Sciences     

Effect of melatonin on antioxidant activity and free radical lipid oxidation in traumatic shock

Effect of melatonin on antioxidant activity and lipid peroxidation in blood, heart, liver, and brain was studied in rats exposed to traumatic shock. Melatonin exerted a potent modulatory effect on antioxidant enzyme activity. Its efficacy depended on organ sensitivity to oxygen deficiency under conditions of traumatic shock. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 4, pp. 387–391, April, 1999.     

Lipid peroxidation in the brain of rats differing in resistance to emotional stress

It is found for each of the rat brain regions studied (cerebral cortex, subjacent white substance, and brainstem) that both the initial levels of 2-thiobarbituric acid-reactive products and the rates of their increment are highest in rats resistant to emotional stress and lowest in stress-prone rats, and that the rates at which lipid peroxidation products accumulate are highest in the brainstem and lowest in the white substance. A correlation is presumed to exist between individual resistance to cerebral ischemia and the rate of lipid peroxidation in particular brain regions of healthy rats. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, № 10, pp. 384–387, October, 1994     

Phosphoinositide response and alterations in free-radical oxidation in rats with catecholamine-induced cardionecrosis

Vascular spasm, hypertrophy of cardiac muscle cells, and necrotic changes in the myocardial tissue of rats administered norepinephrine in incremental doses over 14 days were accompanied by a considerable activation of lipid peroxidation and a weakening of antioxidant defense during the first 7 days of exposure to this injurious agent. On day 14, despite the greatly increased load of norepinephrine, the concentrations of lipid peroxidation products and the activity of antioxidant enzymes deviated from their control values to a lesser extent than on day 7. A similar change was shown by the concentration of brain tissue phosphatidylinositol-4,5-diphosphate, a source of second messengers, suggesting that the phosphoinositide system of second messengers is involved in the mechanisms whereby the destructive effects of norepinephrine are mitigated. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N ^o 8, pp. 137–139, August, 1995 Presented by I. P. Ashmarin, Member of the Russian Academy of Medical Sciences     

The content of tocopherol and lipid peroxidation products in the tissues of rats with genetically determined hyperproduction of free oxygen radicals

It is shown that at the age of 2–3 months S rats with genetically determined hyperproduction of free radicals have the same content of tocopherol in the heart, epididymal fat, adrenals, liver, and liver mitochondria as Wistar rats but a lower content of plasma tocopherol. At 10–12 months, the tocopherol content in all studied tissues and organs, except the liver, is higher than in young S rats and age-matched Wistar rats. This is regarded as a compensatory response facilitating the stabilization of LPO under conditions of increased free radical formation. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 3, pp. 282–284, March, 1996     

Effect of chorionic gonadotropin on normalization of lipid peroxidation

A study is performed of the effect of chorionic gonadotropin on lipid peroxidation in the liver and myocardium of white rats injected subcutaneously with tetrachloromethane for a long time. Chorionic gonadotropin is shown to reduce the content of diene conjugates and Schiff bases, which suggests an antioxidant effect of the hormone. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N ^o 6, pp. 572–573, June, 1994 Presented by Yu. A. Romanov. Member of the Russian Academy of Medical Sciences.     

Effect of fensuccinal on experimental insulin resistance

The effects of new antioxidant fensuccinal on dexamethasone-induced insulin resistance in rats were studied. Oral administration of fensuccinal in a dose of 25 mg/kg for 2 weeks prevented basal hyperinsulinemia and insulin insensitivity of peripheral tissues. Fensuccinal also attenuated oxidative stress by decreasing the concentrations of primary and secondary lipid peroxidation products in liver homogenates. The ability of fensuccinal to prevent dexamethasone-induced insulin resistance is probably due to its antioxidant properties. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 130, No. 7, pp. 42–44, July, 2000     

Effect of fensuccinal on experimental insulin resistance

The effects of new antioxidant fensuccinal on dexamethasone-induced insulin resistance in rats were studied. Oral administration of fensuccinal in a dose of 25 mg/kg for 2 weeks prevented basal hyperinsulinemia and insulin insensitivity of peripheral tissues. Fensuccinal also attenuated oxidative stress by decreasing the concentrations of primary and secondary lipid peroxidation products in liver homogenates. The ability of fensuccinal to prevent dexamethasone-induced insulin resistance is probably due to its antioxidant properties. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 130, No. 7, pp. 42–44, July, 2000     

Effect of prenatal hypoxia on DNA synthesis in the tracheal epithelium and LPO-AOD system in the lungs of newborn rats

Newborn rats euthanized 24 h after birth were examined. The rats were born to females exposed to chronic hypobaric hypoxia on days 14–19 of gestation. The index of nuclei labeled with³H-thymidine in the tracheal epithelium of newborn rats exposed to prenatal hypoxia was 3 times lower than in the control. The LPO level was higher in posthypoxic animals than in intact rats. Prenatal hypoxia led to the suppression of antioxidant defense in the lungs of newborn rats. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N ^o 5, pp. 531–533, May, 1994     

Free-radical oxidation during experimental pneumonia

Lipid peroxidation in the lungs and plasma of albino rats was studied under normal conditions and during experimental pneumonia. In intact rats the content of lipid peroxidation products and the rate of their accumulation in lung homogenate is lower than in homogenates of other organs. Bivalent iron ions added to blood plasma did not induce chemiluminescence characteristic of lipid peroxidation. Experimental pneumonia intensifies production of active oxygen forms by alveolar macrophages and blood neutrophils and increases the content of lipid peroxidation products in lung homogenate. Combined application of antibiotics and antioxidant (vitamin E) during experimental pneumonia promotes normalization of free-radical oxidation and diminishes morphological alterations in the lungs. Translated fromByulleten' Eksperimental'noi Biologii i Medistiny, Vol. 129, No. 3, pp. 260–264, March, 2000