Functional state of rat cardiomyocytes and blood antioxidant system under psycho-emotional stress

We studied the functionality of the antioxidant system in laboratory rat cardiomyocytes and blood under psycho-emotional stress. It was found that 40-day isolation and violation of diurnal cycle among the animals were accompanied by the intensification of lipid peroxidation process and marked with a reduced activity of antioxidant system enzymes, such as catalase and superoxide dismutase activity. The results suggested that psycho-emotional stress was accompanied by oxidative stress, causing a reduction in the intensity of energy metabolism in cardiomyocytes, which was further strengthened by the fact that the activity of the enzymes involved in ATP synthesis in mitochondria was reduced. Based on the results, we proposed that psychological stress is one of the factors contributing to the development of various cardiac diseases.     

Effect of short-term salt stress on oxidative stress markers and antioxidant enzymes activity in tocopherol-deficient Arabidopsis thaliana plants

Changes of carotenoids and anthocyanins content, lipid peroxidation, and activity of antioxidant enzymes were studied in wild type and tocopherol-deficient lines vte1 and vte4 of Arabidopsis thaliana subjected to 200 mM NaCI during 24 h. The salt stress enhanced the intensity of lipid peroxidation to different extent in all three plant lines. Salt stress resulted in an increase of carotenoid content and activity of catalase, ascorbate peroxidase, guaiacol peroxidase and glutathione reductase in wild type and tocopherol-deficient vte1 mutant. However, the increase in anthocyanins concentration was observed in vte1 mutants only. In vte4 mutant, which contain gamma-tocopherol instead of alpha-tocopherol, the response to salt stress occurred via coordinative action of superoxide dismutase and enzymes of ascorbate-glutathione cycle, in particular, ascorbate peroxidase, glutathione reductase, dehydroascorbate reductase, and glutathione-S-transferase. It can be concluded, that salt stress was accompanied by oxidative stress in three studied lines, however different mechanisms involved in adaptation of wild type and tocopherol-deficient lines to salt stress.     

The effect of cadmium chloride and hydrogen peroxide on the lipid peroxidation and fractional composition of lipids in hepatocytes of rats

The isolated hepatocytes were incubated in the medium, containing cadmium chloride or hydrogen peroxide. Influence of the latter on the intensity of lipid peroxidation and contents of some lipids fractions, as well as viability of hepatocytes in these conditions has been studied. It is shown that under such cultivation conditions the activation of lipid peroxidation in the hepatocytes takes place. Its activation in presence of cadmium chloride was one of the factors of the membranes damage. The changes in the content of some fractions of lipids were similar both under the incubations of the cells with cadmium chloride and hydrogen peroxide. This allows one to suppose that cadmium chloride causes changes in the lipid composition of membranes as a result of intensification of lipid peroxidation.     

Role of photoperiodicity and circadian rhythm of glucocorticoids in synchronizing the fluctuations in free-radical oxidation of lipids in rats

A biphasic circadian rhythm in the content of liver lipid peroxidation products has been demonstrated in male Wistar rats housed under the conditions of 12L: 12D, with 3 hours of morning and evening twilight. Maxima of the concentration of the products were observed in the morning and early at night. The rhythm of lipid anti-oxidative activity was found in an anti-phase. Inversion of both the L: D cycle and glucocorticoid circadian rhythms (cortisol injections) led after 14-16 days to the same shifts in the rhythm of anti-oxidative activity. The data indicate that glucocorticoids modulate the diurnal rhythms of lipid anti-oxidative activity and may be responsible for the shifts in the rhythms of free radical oxidation, induced by inversion of the L: D cycle.     

Lipid peroxidation and function of some antioxidant enzyme systems in corn and oats in acute injury by hydrogen fluoride

Experimental research showed the HF main harmful effect at the maximal exposure time (12 h). Intensity of chemiluminescence processes was enhanced almost in 1.5-fold. In the maize leaves the reduced chemiluminescence intensity was observed under the maximal toxicant concentration (1 mg/m3) effect, whereas the further growth of chemiluminescence intensity was observed in the oat plants. The total amount of the lipid peroxidation products was increased dependently on the toxicant concentration in all experimental variants. Changes in the studied enzymatic system activities were multidirected. Analysis of all activities dynamics for the SOD, GGTP, GST, GR and GP showed that GGTP and sometimes GP were involved more rapidly then SOD into the processes of detoxication of lipid peroxidation products and metabolites formed under the HF effect. However, the correlation between changes both in the SOD and GP activities failed to be found. The obtained data give a basis to conclude that during period between 8 and 12 h of HF exposure the essential changes in the activities of SOD and glutathione enzymatic systems took place as an adaptive response of plant cell to the investigated stress-factor impact.     

Age-related peculiarities of antioxidant system functioning in the blood of ostriches

The intensity of lipid peroxidation, activity of some enzymes antioxidant system - superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, amount of recovered glutathione and ceruloplasmin in the blood serum of ostriches in a period from 6- to 60-month age were first investigated. The increase of concentration of lipid peroxidation products is accompanied by the decline of amount of general lipids in the ostriches blood. Every life cycle period of ostriches is characterized by the indexes of functioning of the antioxidant system and intensity of accumulation intermediate lipid peroxidation products inherent in it. The pubescence period and intensive oviposition are characterized by the increase of products lipid peroxidation concentration and decrease of antioxidant enzymes activity, which can testify to the exhaustion of protective possibilities of enzymatic link of antioxidant defence.     

Response of senescing cotyledons of clusterbean to water stress in moderate and low light: Possible photoprotective role of beta-carotene

Senescence of clusterbean ( Cyamopsis tetragonoloba L.) cotyledons in moderate light (12 W m⁻²) brings about a loss in the pigments, enhanced lipid peroxidation and a decline in PS II photochemical activity without any loss either in Dl protein or in the level of β -carotene. The senescence syndrome is aggravated in the cotyledons of water-stressed seedlings with an increase in thylakoid lipid peroxidation, a decline in the level of β -carotene and a quantitative loss in the Dl protein. Loss of the protein, however, is arrested in the seedlings experiencing water stress at low light (3 W m⁻²) intensity that correlates with the stability in the level of β - carotene and a slow rate of lipid peroxidation. Loss of the protein in moderate light is attributed to water-stress sensitized photoinhibitory damage. The data on changes in the components of xanthophyll cycle suggest the low activity of the cycle both during senescence and water stress. It is, therefore, concluded that β -carotene may contribute to the assembly and stability of the Dl protein during senescence and water stress in clusterbean cotyledons.     

The state of peroxidation processes in the basal nuclei of the brain under conditions of an altered photoperiod

The state ofperoxidation processes in the basal nuclei (the nucleus caudatus, globus pallidus, nucleus accumbens, amigdaloid complex) of the rat's brain under conditions of an altered photoperiod has been studied. A disturbance of regular photoperiodicity was shown to result in metabolic changes in the mentioned structures of the brain. Enhancement of the processes of lipid and protein peroxidation was observed in the basal nuclei under constant light, the intensity of fibrinolysis and proteolysis increases, the activity of the enzymes of antioxidant defense decreases. Heterodirectional changes of fibrinolysis and proteolysis in individual structures, a decrease of free radical processes against a background of accumulation of modified proteins were observed under conditions of constant darkness.     

Blood metalloproteins of pro-oxidant and antioxidant action in psoriasis]

Molecular mechanism of pathogenesis of psoriasis related with intensity of formation of oxygen active forms high concentration, depends on balance of pro-oxidant and antioxidant systems activity and leads to quantitative changes of toxic agents of peroxidation processes in blood. Observed results show disorders in Cu, Zn-superoxide dismutase activity and contents of ceruloplasmin, transferrin and new revealed pro-oxidant metalloproteins-cytochromes b558(III), b558(IV), b5, O2(-)-generating lipoprotein suprol and indicate of disturbances in intensity of lipid peroxidation processes. They are considered as obligatory but not specific link in molecular mechanisms of different etiology of oxidative stress formation being as important argument in pathogenesis of various diseases as well as psoriasis.     

Effects of coenzyme Q10 treatment on antioxidant pathways in normal and streptozotocin-induced diabetic rats

Coenzyme Q10 is an endogenous lipid soluble antioxidant. Because oxidant stress may exacerbate some complications of diabetes mellitus, this study investigated the effects of subacute treatment with exogenous coenzyme Q10 (10 mg/kg/day, i.p. for 14 days) on tissue antioxidant defenses in 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione contents, and activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. All tissues from diabetic animals exhibited increased oxidative stress and disturbances in antioxidant defense when compared with normal controls. Treatment with the lipophilic compound coenzyme Q10 reversed diabetic effects on hepatic glutathione peroxidase activity, on renal superoxide dismutase activity, on cardiac lipid peroxidation, and on oxidized glutathione concentration in brain. However, treatment with coenzyme Q10 also exacerbated the increase in cardiac catalase activity, which was already elevated by diabetes, further decreased hepatic glutathione reductase activity, augmented the increase in hepatic lipid peroxidation, and further increased glutathione peroxidase activity in the heart and brain of diabetic animals. Subacute dosing with coenzyme Q10 ameliorated some of the diabetes-induced changes in oxidative stress. However, exacerbation of several diabetes-related effects was also observed.     

Lipid peroxidation associated cardiolipin loss and membrane depolarization in rat brain mitochondria

Oxidative stress induced by Fe2+ (50 microM) and ascorbate (2 mM) in isolated rat brain mitochondria incubated in vitro leads to an enhanced lipid peroxidation, cardiolipin loss and an increased formation of protein carbonyls. These changes are associated with a loss of mitochondrial membrane potential (depolarization) and an impaired activity of electron transport chain (ETC) as measured by MTT reduction assay. Butylated hydroxytoluene (0.2 mM), an inhibitor of lipid peroxidation, can prevent significantly the loss of cardiolipin, the increased protein carbonyl formation and the decrease in mitochondrial membrane potential induced by Fe2+ and ascorbate, implying that the changes are secondary to membrane lipid peroxidation. However, iron-ascorbate induced impairment of mitochondrial ETC activity is apparently independent of lipid peroxidation process. The structural and functional derangement of mitochondria induced by oxidative stress as reported here may have implications in neuronal damage associated with brain aging and neurodegenerative disorders.     

Features of lipid peroxidation in brain and liver tissues from aging rats under stress

The lipid peroxidation (LPO) level between in the adult and old rats brain and liver was determined as to be essentially undiffering. Stress activated the LPO independence the age of animals and tissues investigated. The concentration changes of LPO products testify to it. In the adult rats under the stress capability of tissues to induction in vitro ferment and ascorbat-depending LPO, in comparison with the control, decreases, at old--does not change in the brain and considerably grows in the liver. Stress is accompanied by an oppression of Na, K-ATP-ase PM activity of hepatocytes, more expressed in the old animals.     

Increased brain Na, K-ATPase activity of rats under stress

The activities of Na, K- and Mg-dependent ATPases were measured in crude synaptosomal fractions isolated from the rat brain gray matter. Prolonged (6 h) exposure to emotional painful stress stimulated Na, K-ATPase activity by 40% without affecting that of Mg-ATPase. Preliminary injection of the free radical scavenger ionol presented Na, K-ATPase activation, thus suggesting the involvement of lipid peroxidation initiated in brain tissues under stress in acceleration of NA-pump function. However, model studies with lipid peroxidation induced in vitro by an ascorbate-dependent system in a membranous suspension demonstrated an opposite effect, i. e. fast inhibition of Na, K-ATPase. Possible reasons for the different effects of lipid peroxidation in vivo under stress and on Na, K-ATPase activity in vitro are discussed. It is concluded that activation of Na K-ATPase is a mechanism which is responsible for acceleration of reflex conditioning and for the maintenance of the conditioned reflexes in stress-exposed animals.     

Inhibition of free-radical lipid oxidation in the mechanisms of immediate and long-term adaptation to stress

The literary data and own results concerning the stages of free radical lipid oxidation inhibition during the adaptation of animals to stress are reviewed. Using the chronic stress models such as immobilization, experimental neurosis, it has been shown, that in general adaptation syndrome the stage of permanent adaptation to stress corresponds to a permanent inhibition of free radical processes in animal tissues. This stage is accompanied by the activation of superoxide radical scavenging and corresponding changes of lipid composition. similar results are obtained on the model of the development of permanent compensation processes after brain injury. Studying the acute stress it has been found, that during first minutes the inhibition of lipid peroxidation which precedes its further activation takes place. This stage corresponds to the realization of urgent adaptation phase to stress. The role of inhibition of free radical processes in mechanisms of urgent and permanent adaptation to stress is under discussion.     

Selective suppression of lipid peroxidation in the brain under stress

The time course of lipid peroxidation (LP) products was studied in the heart, liver, and brain of rats exposed to 1, 6 and 12 h stress and compared with the extent of LP induction in these organs in vitro. It was shown that the LP activation in the internal organs with maximum in 1 h stress was accompanied by 2 fold decrease in LP products in the brain. More prolonged stress eliminated differences between tissues in all organs approaching the LP level to the control. The LP induction in vitro also revealed reciprocal relations between the LP intensity in brain and internal organs which remained in control group as well. Possible role of the LP suppression in brain induced by acute stress and significance of the phenomenon are under discussion.     

Effect of litonit and teturam on the course of biochemical processes in infectious inflammatory lesions of the kidneys in alcoholized animals

The time-course of changes in the activity of sorbitol dehydrogenase, catalase and the intensity of lipid peroxidation in the blood and kidneys of 250 albino rats was studied in the course of the development of alcoholic dependence when suffering from secondary infection. Litonit, a new antialcoholic drug, was found to be effective for the treatment of infectious inflammatory renal lesions in alcoholism. Unlike teturam, litonit promoted the decrease of sorbitol dehydrogenase and catalase activity in the kidneys and abated the intensity of lipid peroxidation. The possibility of using litonit as one of the remedies of pathogenetic therapy for infectious inflammatory renal lesions in alcoholism is under discussion.     

Changes in Sphingomyelinase Activity,Tumor Necrosis Factor α Level,and Lipid Peroxidation Intensity in the Course of Development of Cholestatic Liver Injury

Changes in sphingomyelinase activity, tumor necrosis factor α expression, and level of lipid peroxidation products in the course of development of cholestatic liver injury have been studied. The same type phase shifts in the analyzed parameters were observed, which included a marked decrease at the early stages of cholestasis (days 3–6) and a pronounced increase at the later stages (days 12–16), i.e., under the conditions of developed pathology. There was a significant positive linear correlation between tumor necrosis factor α expression, sphingomyelinase activity, and lipid peroxidation intensity in cholestatic injury. We propose that detected changes may reflect the balance between the effects of the two major bile components—bilirubin, which is accumulated in the liver at the early stages of cholestasis, and bile acids, whose influence dominates at the later stages of pathologic process. Our results indicate that tumor necrosis factor α overexpression, sphingomyelin cycle activation, and lipid peroxidation intensification may cause apoptosis of hepatocytes at the late stages of cholestasis.     

干旱胁迫对坡柳等抗旱树种幼苗膜脂过氧化及保护酶活性的影响

以金沙江干热河谷主要树种坡柳、银合欢、山毛豆实生幼苗为材料,通过盆栽苗自然干旱胁迫,同时以浇水处理为对照,研究了干旱胁迫对坡柳、银合欢、山毛豆3个树种丙二醛含量、膜相对透性及保护酶活性的影响。结果表明,干旱胁迫下3个树种幼苗的细胞膜透性、MDA及SOD, POD酶活性都发生了变化,只是变化的幅度和进程不同。干旱胁迫对银合欢膜系统损伤生成的主要降解产物不是MDA;山毛豆清除活性氧毒害作用主要不是通过SOD和POD的作用;通过叶片相对保水力测定及膜透性、MDA相对含量、酶活性变化情况的分析,3个树种中坡柳耐旱性最强,其次为银合欢,山毛豆居后。     

Effect of L-arginine and N(omega)-nitro-L-arginine on oxidative phosphorylation and lipid peroxidation in rats with various tolerance to hypoxia under stressful conditions

The influence of L-arginine (600 mg/kg) and NO-synthase blocator N omega-nitro-L-arginine L-NNA (35 mg/kg) on processes of ADP-stimulated respiration (under using 0.35 mM succinate, 1 mM alpha-ketoglutarate, 2 mM pyruvate, 2 mM glutamate, 2 Mm malate and succinate dehydrohenase blocator--2 mM malonate as substrates of oxidation), lipid peroxidation (concentration of DK and MDA), activities of succinate dehydrohenase and aminotransferases in rats tissues with different resistance to hypoxia under stress conditions have been investigated. It have been shown that the energy metabolism indices (respiration rate and efficiency of phosphorilation ADP/O) are higher in high resistent (HR) animals in the control group. Stress causes the increase of ADP-stimulated respiration in low resistent (LR) under succinate oxidation and decrease of NADPH-dependent utilization, indicative of more effort of energy system in LR animals. Stress conditions are connected with the increase of lipid peroxidation products in blood both in LR and in HR animals, though in hepar their concentration change unimportantly. Injection of L-arginine decreases aerobic component of energy metabolism on the background decreasing aminotransferases ways of oxidation and succinate dehydrohenase activity. L-arginine causes decrease of lipid peroxidation products in LR, in HR the same effect reaches by L-NNA injection. The has been made conclusion about tight correlation between energy metabolism, processes of lipid peroxidation with resistance to hypoxia and functioning of nitric oxide cycle under stress conditions.     

Regional effects of ageing on Na+,K(+)-ATPase activity in rat brain and correlation with multiple unit action potentials and lipid peroxidation.

Effects of ageing on Na+,K(+)-ATPase activity in crude synaptosomal fractions from the rat brain parietal cortex, hippocampus, striatum and thalamus has been studied. From 12 months to 24 months, a progressive decline in enzyme activity in the parietal cortex, hippocampus and striatum was found which correlated with increase in lipid peroxidation in the three brain regions. In the thalamus, ageing did not affect the enzyme activity and lipid peroxidation. Age-related decline in multiple unit action potentials was also observed in two brain regions, viz. hippocampus and parietal cortex. Statistical correlations calculated by Pearson's correlation coefficient showed that decline in Na+,K(+)-ATPase activity correlated to decline in multiple unit action potentials. There was rise in lipid peroxidation also and the data indicate that age-related changes in lipid peroxidation and Na+,K(+)-ATPase activity contribute to the deterioration of electrophysiological activity.