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.     

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.     

Tissue specificity of lipid peroxidation under emotional stress in rats

The intensity of lipid peroxidation and activity of antioxidant system enzymes in the blood plasma, brain and cardial muscle of laboratory rats under 40 days of isolation and violation of diurnal cycle was studied. The obtained data show that on the background of concentration changes in NO changes also take place in the intensity of lipid peroxidation process, indicated by changes in the concentration of TBA-active products and diene conjugates. The changes taking place in the activity of superoxidedismutase, catalase, succinatdehydrogenase, creatine kinase and aldolase under stress were studied. The resulting data show that isolation of animals and violation of diurnal cycle are the factors causing a significant reduction in the energy metabolism in the brain and heart tissue cells and resulting in oxidative stress that, in its turn, may become the reason for development of toxic radicals. Furthermore, prolonged stress may result in irreversible processes that are considered to be the reasons for significant pathologies of the cardiovascular system.     

Effects of acute manganese chloride exposure on lipid peroxidation and alteration of trace metals in rat brain

Although manganese (Mn) is an essential element, exposure to excessive levels of Mn and its accumulation in the brain can cause neurotoxicity and extrapyramidal syndrome. We have investigated the differences in the accumulated levels of Mn, the degree of lipid peroxidation, and its effects on the levels of trace elements (Fe, Cu, and Zn) in various regions in the brain of rats having undergone acute Mn exposure. The rats in the dose—effect group were injected intraperitoneally (ip) with MnCl₂ (25, 50, or 100 mg MnCl₂/kg) once a day for 24 h. The Mn significantly accumulated (p<0.05) in the frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus medulla, cerebellum, and spinal cord in each case. The rats in the timecourse group were ip injected with MnCl₂ (50 mg MnCl₂/kg) and then monitored 12, 24, 48, and 72 h after exposure. The Mn accumulated in the frontal cortex, corpus callosum, hippocampus, striatum hypothalamus, medulla, cerebellum, and spinal cord after these periods of time, In both the dose—effect and time-course studies, we observed that the concentration of malondialdehyde, an end product of lipid peroxidation, increased significantly in the frontal cortex, hippocampus, striatum, hypothalamus, medulla, and cerebellum. However, no relationship between the concentrations of Mn in the brain and the extent of lipid peroxidation was observed. In addition, we found that there was a significant increase (p<0.05) in the level of Fe in the hippocampus, striatum, hypothalamus, medulla, and cerebellum, but the Cu and Zn levels had not changed significantly. These findings indicated that Mn induces an increase in the iron level, which provides direct evidence for Fe-mediated lipid peroxidation in the rats' brains; these phenomena might play important roles in the mechanisms of Mn-induced neurotoxicology.     

Studies on lipid peroxidation in the rat brain

The aim of this study was to set up a simple procedure for assessing lipid peroxidation (L.P.) and testing the activity of antioxidant compounds. L. P. was determined in rat brain homogenates by measuring the endogenous and stimulated accumulation of malonaldehyde (MDA). MDA was assayed by an HPLC method. Homogenates spontaneously formed appreciable amounts of MDA. The addition of increasing concentrations of FeCl₂ resulted in a linear accumulation of MDA, up to 16.6-fold at 50 M. An organic form of iron (Fe-saccharate) was less active on MDA formation (11.4-fold increase at 100 M). The addition of xanthine-xanthine oxidase resulted in only a 2.4-fold increase in MDA formation. Various antioxidant or chelating compounds effectively inhibited L.P., with IC₅₀ between 0.1 M (phenoxazine) and 4–50 M (-tocopherol). Their potencies depended on the iron concentration and time of preincubation with the homogenates. In conclusion, this is a simple and reliable procedure for studying L.P. and inhibiting agents, provided that the experimental conditions are carefully assessed.     

Effect of brain antibodies on the lipid peroxidation process in the brain

The authors studies the effects of blood serum and IgG fraction from dogs immunized with brain and blood sera from patients with multiple sclerosis and schizophrenia on lipid peroxidation in rat brain homogenates. Measured the content of diene conjugates (DC) and malonic dialdehyde (MDA) in the rat brain after administering the IgG fraction. It was established that antioxidant activity of blood sera and IgG fraction from control animals and donors was significantly higher as compared to experimental. Administration of the IgG fraction brought about an increase in the content of DC and MDA in the brain of experimental animals. It is concluded that complement-dependent brain antibodies present in the blood serum of patients with schizophrenia and multiple sclerosis potentiate lipid peroxidation in the cerebral tissue and that the unsophisticated and informative method for antibody determination may be used in clinical practice.     

Carbon monoxide-mediated brain lipid peroxidation in the rat

Clinical and animal data suggest that the pathogenesis of CO poisoning extends beyond the inhibition of hemoglobin function, but no mechanism has been identified. Evidence of neurological compromise, particularly loss of consciousness, has been implicated as a marker for increased mortality and morbidity in clinical reports. Experiments were carried out with rats to assess whether CO exposure may cause brain lipid peroxidation. With the use of two methods, measurement of conjugated dienes and thiobarbituric acid reactivity, brain lipid peroxidation could be documented as a result of exposure to CO at a concentration sufficient to cause unconsciousness. Products of lipid peroxidation were increased by 75% over the base-line values 90 min after CO exposure. Unconsciousness was associated with a brief period of hypotension, so brief that in itself it caused no apparent insult. Lipid peroxidation occurred only after the animals were returned to CO-free air, and there was no direct correlation with the carboxyhemoglobin level. This work may provide an explanation for a number of currently poorly understood clinical observations regarding CO poisoning.     

Effects of cadmium-metallothionein on renal organic ion transport and lipid peroxidation in rats

The effects of cadmium-metallothionein (Cd-MT) on organic ion uptake in renal cortical slices and lipid peroxidation in the kidney were studied in rats. For in vitro studies, slices were prepared from kidneys of control animals and incubated in buffer containing either cadmium chloride (CdCl₂) or Cd-MT in equimolar Cd concentrations ranging from 5 × 10^?6 to 2 × 10^?4 M. Uptake into the slices of the organic anion p-aminohippuric acid (PAH) was found to be inhibited by both forms of Cd in a dose-dependent manner. Although this inhibition was slightly greater in the presence of Cd-MT, accumulation of Cd into the slices was approximately 12 times greater with CdCl₂ than Cd-MT. Tetraethylammonium (TEA) uptake was less sensitive to the inhibitory effects of both CdCl₂ and Cd-MT, although a dose-dependent inhibition did occur with higher Cd concentrations. To study the in vivo effects of Cd-MT on transport function and lipid peroxidation in the kidney, rats were injected with Cd-MT (0.3 mg Cd per kilogram body weight [bw]) and sacrificed at specific time intervals. Similar to the in vitro studies, PAH uptake into the renal cortical slices was markedly inhibited within 12 hours after Cd-MT injection whereas inhibition of TEA uptake was less and not observed until 48 hours after injection. Only a small increase (1.4-fold) in lipid peroxidation, as measured by generation of malondialdehyde (MDA), in the kidney was detected at four hours postinjection, and no further increase was observed at later time periods. The results suggest that Cd-MT affects the transport of organic anions and cations during its renal uptake but that lipid peroxidation may play only a minor role in Cd-MT-induced renal toxicity.     

The lipid peroxidation system in the retina and brain of rats during early postnatal ontogeny

The content of the lipid peroxidation products in the rat retina and brain tissues during the early postnatal period (20-45 day of life) was estimated. It was shown during this period the content of conjugated dienes was decreased: the content of malondialdehyde and Schiff bases was without changes in the rat retina. At the same time the content of the conjugated dienes and Schiff bases in the brain tissue was proportionally increased. The activity of glutathioneperoxidase and glutathionereductase was decreased in the retina and not changed in brain. In the same period of the life the content of alpha-tocopherol in the retina was increased. We observed also the enhance of the rate of the induced lipid peroxidation in brain and retina of older animals.     

Sensitivity to in vitro lipid peroxidation in liver and brain of aged rats.

Lipid peroxidation in rat liver and brain has been studied to see if it increases with old age. No significant differences in the level of endogenous, nonstimulated lipid peroxidation (TBA-RS) is found between 9 month-old (mature adults) and 28 month-old animals in liver or cerebral cortex. Liver homogenates subjected in vitro to an oxidative stress (ascorbate-Fe++), show a clearly slower peroxidation rate in old than in young animals. On the other hand, the in vitro peroxidation rate of cerebral homogenates was similar in young and old animals. The in vitro peroxidation rate was much higher in brain than in liver tissue. These results do not support the view that old rats liver and brain are more susceptible to free radical oxidative damage than those of young ones.     

Effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration,ROS production and lipid peroxidation in broiler chickens

In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25 °C (relative humidity, RH, 70 ± 5%) for 6 d and subsequently exposed to 35 °C (RH, 70 ± 5%) for 3 h, then the heat stress was removed and the temperature returned to 25 °C (RH, 70 ± 5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12 h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12 h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner.     

小茴香对肝纤维化大鼠脂质过氧化水平的影响

目的：研究小茴香对肝纤维化大鼠的脂质过氧化水平的影响。方法：取Wister大鼠100只,随机取12只设为正常组,其余采用四氯化碳（CCL4）复合因素法复制肝纤维化大鼠模型,复制成功后随机分为模型对照组、小茴香组和复方丹参组（n=12）;相应药物干预8周后,镜检肝组织形态学改变;全自动生化分析仪检测外周血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）水平与血清总蛋白（TP）、白蛋白（ALB）含量;生化法检测肝组织羟脯氨酸（HYP）与血清丙二醛（MDA）含量及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—PX）、过氧化氢酶（CAT）活性。结果：HE结果显示：模型组肝脏炎症与脂肪变性明显,经小茴香干预后明显改善。生化检测结果显示：与正常组比较,模型组ALT、AST水平显著升高（P〈0．05）,TP、ALB含量显著降低（P〈O．05）,HYP、MDA含量显著增加（P〈0．05）,而SOD、GSH—PX和CAT活性显著降低（P〈0．05）;与模型组比较,小茴香组ALT、AST水平显著下降（P〈0．05）,TP、ALB水平显著升高（P〈0．05）;HYP、MDA含量显著降低（P〈0．05）,SOD、GSH—PX和CAT活性显著提高（P〈0．05）。结论：小茴香的抗肝纤维化作用可能与调节大鼠脂质过氧化水平有关。     

小茴香对肝纤维化大鼠脂质过氧化水平的影响

目的:研究小茴香对肝纤维化大鼠的脂质过氧化水平的影响。方法:取Wister大鼠100只,随机取12只设为正常组,其余采用四氯化碳(CCL4)复合因素法复制肝纤维化大鼠模型,复制成功后随机分为模型对照组、小茴香组和复方丹参组(n=12);相应药物干预8周后,镜检肝组织形态学改变;全自动生化分析仪检测外周血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平与血清总蛋白(TP)、白蛋白(ALB)含量;生化法检测肝组织羟脯氨酸(HYP)与血清丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、过氧化氢酶(CAT)活性。结果:HE结果显示:模型组肝脏炎症与脂肪变性明显,经小茴香干预后明显改善。生化检测结果显示:与正常组比较,模型组ALT、AST水平显著升高(P<0.05),TP、ALB含量显著降低(P<0.05),HYP、MDA含量显著增加(P<0.05),而SOD、GSH-PX和CAT活性显著降低(P<0.05);与模型组比较,小茴香组ALT、AST水平显著下降(P<0.05),TP、ALB水平显著升高(P<0.05);HYP、MDA含量显著降低(P<0.05),SOD、GSH-PX和CAT活性显著提高(P<0.05)。结论:小茴香的抗肝纤维化作用可能与调节大鼠脂质过氧化水平有关。     

Activation of lipid peroxidation in the brain in cerebral hemorrhage

The effect of intracerebral hemorrhage (injection of 0.15 ml of autogenic blood during 2 min in capsula interna) on lipid peroxidation in brain tissue was studied in rat experiments. Intracerebral hemorrhage resulted in a progressive increase of conjugated diene and malonic dialdehyde concentrations, and a decrease in the levels of cerebral lipids antiradical activity. This effect appeared by the 3-rd hour and was significantly manifest 24 hours after the blood injection into the brain.     

Hypoxia-induced lipid peroxidation in the brain during postnatal ontogenesis

Reactive oxygen species (ROS) are common products of the physiological metabolic reactions, which are associated with cell signaling and with the pathogenesis of various nervous disorders. The brain tissue has the high rate of oxidative metabolic activity, high concentration of polyunsaturated fatty acids in membrane lipids, presence of iron ions and low capacity of antioxidant enzymes, which makes the brain very susceptible to ROS action and lipid peroxidation formation. Membranes of brain cortex show a higher production of thiobarbituric acid-reactive substances (TBARS) in prooxidant system (ADP.Fe(3+)/NADPH) than membranes from the heart or kidney. Lipid peroxidation influences numerous cellular functions through membrane-bound receptors or enzymes. The rate of brain cortex Na(+),K(+)-ATPase inhibition correlates well with the increase of TBARS or conjugated dienes and with changes of membrane fluidity. The experimental model of short-term hypoxia (simulating an altitude of 9000 m for 30 min) shows remarkable increase in TBARS in four different parts of the rat brain (cortex, subcortical structures, cerebellum and medulla oblongata) during the postnatal development of Wistar rat of both sexes. Young rats and males are more sensitive to oxygen changes than adult rats and females, respectively. Under normoxia or hypobaric hypoxia both ontogenetic aspects and sex differences play a major role in establishing the activity of erythrocyte catalase, which is an important part of the antioxidant defense of the organism. Rats pretreated with L-carnitine (and its derivatives) have lower TBARS levels after the exposure to hypobaric hypoxia. The protective effect of L-carnitine is comparable with the effect of tocopherol, well-known reactive species scavenger. Moreover, the plasma lactate increases after a short-term hypobaric hypoxia and decreases in L-carnitine pretreated rats. Acute hypobaric hypoxia and/or L-carnitine-pretreatment modify serum but not brain lactate dehydrogenase activity. The obtained data seem to be important because the variations in oxygen tension represent specific signals of regulating the activity of many specific systems in the organism.     

水分胁迫对黄檗幼苗保护酶活性及脂质过氧化作用的影响

以轻度干旱、重度干旱和水涝处理黄檗幼苗,测定丙二醛(MDA)和游离脯氨酸含量及超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性的动态变化.结果表明,处理40 d以后,轻度干旱、重度干旱和水涝处理的叶片MDA含量始终显著高于对照,最高分别达对照的2.9、2.37和4.12倍,三者之间在处理80 d以后MDA含量差异不显著.水涝处理和对照的游离脯氨酸含量在处理期间没有明显变化,干旱处理的游离脯氨酸含量从处理后40 d开始增加、80 d后回落,重度干旱处理的增加幅度显著大于轻度干旱处理.SOD、POD和CAT活性的变化趋势缺乏一致性,但重度干旱处理的黄檗幼苗,叶片的SOD、POD和CAT活性在处理期间始终显著高于轻度干旱、水涝处理和对照.     

Diaphragmatic lipid peroxidation in chronically loaded rats

Recent workindicates that free radical-mediated lipid peroxidation takes placewithin the diaphragm on strenuous contraction. This phenomenon has onlybeen demonstrated using fairly artificial experimental models and hasnot been studied during the type of sustained respiratory loadingtypically seen in patients with lung disease. The purpose of thepresent study was to measure the levels of several biochemical markersof protein oxidation (protein carbonyl levels) and lipid peroxidation(8-isoprostane, reduced glutathione, and oxidized glutathione levels)in diaphragms of rats subjected to chronic respiratory loading.Respiratory loading was accomplished by tracheal banding; groups ofanimals were loaded for 4, 8, or 12 days, and a group of sham-operated unloaded animals was used as controls. After loading, animals werekilled, diaphragm contractility was assessed in vitro by using aportion of the excised diaphragm, and the remaining diaphragm and thesoleus muscles were used for biochemical analysis. We found diminishedforce generation in diaphragms from all groups of banded animalscompared with muscles from controls. For example, twitch force averaged7.8 ± 0.8 (SE) N/cm² inunloaded animals and 4.0 ± 0.4, 3.0 ± 0.4, and 3.4 ± 0.4 N/cm² in animals loaded for 4, 8, and 12 days, respectively (P < 0.0001). Loading also elicited increases in diaphragmatic proteincarbonyl concentrations (P < 0.001),and the time course of alterations in carbonyl levels paralleledloading-induced alterations in the diaphragm force-frequencyrelationship. Although loading was also associated with increases indiaphragmatic 8-isoprostane levels (P < 0.003) and reductions in diaphragm reduced glutathione levels (P < 0.003), the time course ofchanges in these latter parameters did not correspond to alterations inforce. Soleus glutathione and carbonyl levels were not altered bybanding. We speculate that respiratory loading-induced alterations indiaphragmatic force generation may be related to free radical-mediatedprotein oxidation, but not to free radical-induced lipid peroxidation.     

镉胁迫对平邑甜茶脂肪酸构成及脂质过氧化的影响

以平邑甜茶幼苗为试材,研究了镉胁迫下幼苗叶片和根系膜脂肪酸构成、活性氧、脂氧合酶和丙二醛含量的变化.结果表明：氯化镉处理后7～12 h,脂肪酸种类及其相对含量变化最为明显.处理后7 h,叶片和根系脂肪酸不饱和水平升至最高,含量分别达8282%和7243%;叶片可检测到的脂肪酸在处理后12 h由11种增至14种,根系则在处理17 h后由4种增至6种.O₂^.-产生速率在处理3 h、H₂O₂含量在处理7 h时升至最高,丙二醛含量和脂氧合酶活性则随着处理时间的延长逐渐增加.镉胁迫通过诱导活性氧和脂氧合酶来改变平邑甜茶脂肪酸构成,并引起脂质过氧化;镉处理12 h前,脂质过氧化是活性氧和脂氧合酶的共同结果;但处理12 h后,脂质过氧化加剧主要在于脂氧合酶活性的持续增加.