Effects of Acrylamide on the Nervous Tissue Antioxidant System and Sciatic Nerve Electrophysiology in the Rat

To investigate the time-dependent effects of acrylamide (ACR) on the antioxidative status in rat nerve tissues, adult male Wistar rats were given ACR (40 mg/kg, i.p., 3 times/week) for 2, 4, 6 and 10 weeks, respectively. The time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues were investigated. The electrophysiology indices (nerve conduction velocity, NCV; compound action potential duration, CAPD; compound action potential amplitude, CAPA; compound action potential latency, CAPL) in the sciatic nerve were determined using BL-420E Biologic Function Determining System. The results showed that MDA levels increased significantly (P < 0.05) in nerve tissues, while GSH levels markedly decreased (P < 0.05) in a time-dependent manner. SOD activity (in the spinal cord and sciatic nerve) and GR activity (in the sciatic nerve) increased significantly after 4 weeks ACR treatment (P < 0.01), but then decreased (P < 0.05). The anti-ROS activity in the sciatic nerve was markedly decreased at the end of week 6 and 10 (P < 0.01). The above indices changed most in the sciatic nerve. The levels of GSH, MDA and anti-ROS in rat sciatic nerve were in high correlation (P < 0.05, |r| > 0.80) with the electrophysiology indices according to the exposure time. Thus, ACR-induced neurotoxicity may be associated with the enhancement of lipid peroxidation and reduction of the antioxidative capacity. Depletion of neural GSH level might be one of the primary events in ACR-induced neuropathy. Ying-Jian Zhu and Tao Zeng––These authors contributed equally to this work.     

Lipid Peroxidation was Involved in the Memory Impairment of Carbon Monoxide-induced Delayed Neuron Damage

Carbon monoxide (CO)-induced delayed neuron damage is the serious complication, but the underlying mechanisms are poorly understood. This study was designed to investigate the time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; and anti-reactive oxygen species anti-ROS) in nerve tissues for the possible mechanisms exploration. Adult rats were treated with CO by peritoneal injection, and sacrificed after day 0, 1, 3, 7, 14 and 21 of treatment. The results showed that the step-down latency progressively shortened while the numbers of error increased. Comparing with the level of day 0, MDA levels in serum, cerebral cortex and hippocampus significantly increased on day 1, 3 and 7. The level of GSH increased firstly but then decreased. The activities of GR, GSH-Px, and anti-ROS decreased in serum, cerebral cortex and hippocampus of rats after day 1, 3, 7, 14 and 21. Thus, we concluded that CO-mediated delayed neuron damage might be associated with elevation of lipid peroxidation and reduction of antioxidative status. The time-dependent changes of lipid peroxidation and antioxidative status in serum, cerebral cortex and hippocampus, at least in part, are involved in the toxic effects of CO poisoning on neuron.     

Changes in Rapid Transport of Phospholipids in the Rat Sciatic Nerve During Axonal Regeneration

Abstract: Axonal transport of phospholipids in normal and regenerating sciatic nerve of the rat was studied. At various intervals after axotomy of the right sciatic nerve in the midthigh region and subsequent perineurial sutures of the transected fascicles, a mixture of 60 μCi [Me-^HC]choline and 15 μCi [2-³H]glycerol in the region of the spinal motor neurons of the L5 and L6 segments was injected bilaterally. The amount of radioactive lipid (and in certain cases its distribution in various lipid classes) along the nerve was determined as a function of time. Three days after fascicular suture and 6 h after spinal cord injection of precursors, there was an accumulation of labeled phospholipids and sphingolipids in the transected sciatic nerve in the region immediately proximal to the site of suture. Nine days after, there was a marked increase in the accumulation of radioactivity in the distal segments of the injured nerve, which increased up to 14 days after cutting and disappeared as regeneration proceeded (21–45 days). In all segments of both normal and regenerating nerve fibers, as well as in L5 and L6 spinal cord segments, only phosphatidylcholine and sphingomyelin were labeled with [¹⁴C]choline. These results suggest that the regeneration process in a distal segment of a peripheral neuron, following cutting and fascicular repairing by surgical sutures, is sustained in the first 3 weeks by changes in the amount of phospholipids rapidly transported along the axon towards the site of nerve fiber outgrowth.     

Protective effects of polysaccharide from Euphorbia kansui (Euphorbiaceae) on the swimming exercise-induced oxidative stress in mice

The present study examined the effects of derivatives of galactosides and glucosides in a polysaccharide extract from Euphorbia kansui (Euphorbiaceae) on exercise-induced oxidative stress in mice. Exhaustive swimming exercise significantly increases the degree of lipid peroxidation in terms of malondialdehyde content and reduces the antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Our findings revealed that chronic oral treatment with the extract elevates enzymatic activities of SOD and GPx accompanied by a corresponding decrease in malondialdehyde. The antioxidative activities of these compounds against exercise-induced oxidative stress are correlated with various activities such as reducing the production of superoxide and hydroxyl radicals, inhibiting lipid peroxidation, enhancing antioxidative defenses, and increasing the production of SOD and GPx activity and expression in different tissues. These compounds may be involved in glycogen metabolism to meet the requirement of working skeletal muscles and act as antioxidants by terminating the chain reaction of lipid peroxidation to maintain the morphological stability of mitochondria in spinal motor neurons. These observations suggest that E. kansui has antioxidative and antifatigue properties and can be given as prophylactic and (or) therapeutic supplements for increasing antioxidant enzyme activities and preventing lipid peroxidation during strenuous exercise.     

The effects of aerobic exercise training on the age-related lipid peroxidation, Schwann cell apoptosis and ultrastructural changes in the sciatic nerve of rats

The potential role of exercise in preventing the age-related spontaneous peripheral neuropathy has not been studied. We examined the effects of long-term aerobic exercise training on lipid peroxidation, Schwann cell (SC) apoptosis and ultrastructural changes in the sciatic nerve of rats during aging. Three groups of 12-week old Wistar rats ran on a treadmill for 6, 9 and 12 months (exercise trained (ET) group, n=10 each) according to an exercise training program targeted at a speed of 22 m/min (at 7 degrees incline), 60 min/day, 6 days/week. Three corresponding groups of untrained rats were used as the controls (sedentary (SED) group). At the end of each period, sciatic nerve biopsies were performed, and processed for biochemical, immunohistochemical and ultrastructural analyses. The results showed that aging was associated with an increased level of nerve malondialdehyde (MDA, marker of lipid peroxidation) and a higher number of SC apoptosis in SED group. The SED group showed irregular nerve fibers with thin myelin sheaths and areas of myelin-axon detachment. However, the ET group had significantly diminished nerve lipid peroxidation and SC apoptosis. In the ET group, nerve fibers had a thick myelin sheath with frequent folding. These findings suggest that aerobic exercise training protects peripheral nerves by attenuating oxidative reactions, and preserving SCs and myelin sheath from pathologic changes, which occur during normal aging.     

Retrograde transport of transmissible mink encephalopathy within descending motor tracts

The spread of the abnormal conformation of the prion protein, PrP(Sc), within the spinal cord is central to the pathogenesis of transmissible prion diseases, but the mechanism of transport has not been determined. For this report, the route of transport of the HY strain of transmissible mink encephalopathy (TME), a prion disease of mink, in the central nervous system following unilateral inoculation into the sciatic nerves of Syrian hamsters was investigated. PrP(Sc) was detected at 3 weeks postinfection in the lumbar spinal cord and ascended to the brain at a rate of approximately 3.3 mm per day. At 6 weeks postinfection, PrP(Sc) was detected in the lateral vestibular nucleus and the interposed nucleus of the cerebellum ipsilateral to the site of sciatic nerve inoculation and in the red nucleus contralateral to HY TME inoculation. At 9 weeks postinfection, PrP(Sc) was detected in the contralateral hind limb motor cortex and reticular thalamic nucleus. These patterns of PrP(Sc) brain deposition at various times postinfection were consistent with that of HY TME spread from the sciatic nerve to the lumbar spinal cord followed by transsynaptic spread and retrograde transport to the brain and brain stem along descending spinal tracts (i.e., lateral vestibulospinal, rubrospinal, and corticospinal). The absence of PrP(Sc) from the spleen suggested that the lymphoreticular system does not play a role in neuroinvasion following sciatic nerve infection. The rapid disease onset following sciatic nerve infection demonstrated that HY TME can spread by retrograde transport along specific descending motor pathways of the spinal cord and, as a result, can initially target brain regions that control vestibular and motor functions. The early clinical symptoms of HY TME infection such as head tremor and ataxia were consistent with neuronal damage to these brain areas.     

Astrocytes enhance radical defence in capillary endothelial cells constituting the blood-brain barrier.

Astrocytes (AC) induce blood-brain barrier (BBB) properties in brain endothelial cells (EC). As antioxidative activity (AOA) is assumed to be a BBB characteristic, we tested whether AC improve AOA of EC. Monocultivated AC showed higher AOA [manganese superoxide dismutase (SOD), catalase (Cat), glutathione peroxidase (GPx)] than EC. Cocultivation elevated AOA in EC (MnSOD, CuZnSOD, Cat, GPx), and AC (MnSOD, CuZnSOD, GPx). Hypoxia increased radical-induced membrane lipid peroxidation in monocultivated, but not in cocultivated EC. Thus, EC/AC cocultivation intensifies AOA in both cell types, protects the EC, and therefore, the BBB against oxidative stress. The high AOA is regarded as an essential property of the BBB, which is induced by AC.     

大鼠脊髓诱发电位与脊髓损伤的关系——Ⅲ.脊髓局部损毁后电位的变化及电位来源分析

本文描述了大鼠脊髓L_1节段后柱、后索、侧索和前角的诱发电位及其损伤后的变化,并观察了切断L_4、L_5脊神经背、腹根与横断高位颈髓对电位的影响,以进行行电位来源分析。结果可见,上述四个区域的诱发电位基本由早反应三相波和晚反应组成。分别电解损毁这些部位后,电位波幅均普遍降低,晚期反应较早反应降低明显。后柱或后索受损对电位影响最大。局部损毁后可见L_1及T_(13)水平的硬膜上电位改变明显,尤其晚反应减弱、波峰平坦。反应时值与潜伏时未见明显改变。切断L_4脊神经背、腹根后、电位基本消失。去大脑对电位未见明显影响。结果表明,刺激坐骨神经诱发的脊髓电位起源于低位腰段传入神经和脊髓内多通路的兴奋传导,在一定程度上受腹根逆行活动的影响,与大脑及脊髓下行传导束活动无直接联系。脊髓诱发电位的幅度与波形改变可作为脊髓损伤的判断指标之一。     

Prophylactic effects of magnesium and vitamin E in rat spinal cord radiation damage: evaluation based on lipid peroxidation levels

This study investigated the neuroprotective effects of magnesium sulfate prophylaxis and vitamin E prophylaxis in a rat model of spinal cord radiation injury. Groups were subjected to different treatment conditions for 5 days prior to irradiation, and outcomes were evaluated on the basis of lipid peroxidation levels in cord tissue. Four groups of rats were investigated: no radiation/treatment (n = 4), intraperitoneal (i.p.) saline 1 ml/day (n = 6), i.p. vitamin E 100 mg/kg/day (n = 6), and i.p. magnesium sulfate 600 mg/kg/day (n = 6). The thoracic cord of each non-control rat was exposed to 20 Gy radiation in a LINAC system using 6 MV x-rays, and malondialdehyde (MDA) levels (reflecting lipid peroxidation level) were determined 24 hours post-irradiation. The MDA levels in thoracic cord segments from the control rats were used to determine baseline lipid peroxidation. The mean levels in the control, saline-only, vitamin E, and magnesium sulfate groups were 12.12 +/- 0.63, 27.0 +/- 2.81, 17.71 +/- 0.44, and 14.40 +/- 0.47 nmol/mg tissue, respectively. The MDA levels in the saline-only group were significantly higher than baseline, and the levels in the vitamin E group were significantly lower than those in the saline group (P < 0.05 for both). The levels in the magnesium sulfate group were dramatically lower than those in the saline group (P < 0.001). The results indicate that i.p. magnesium sulfate has a marked neuroprotective effect against radiation-induced oxidative stress in the rat spinal cord.     

神经生长因子对兔坐骨神经损伤后脊髓前角运动神经元乙酰胆碱酯酶的影响

钳夹损伤兔右坐骨神经,于损伤处注射蛇毒ＮＧＦ４００Ｂｕ／ｋｇ／日,损伤术后１,３,７天和２,３,４,６,８周动态观察脊髓腰段伤侧第Ⅸ板层外侧群的大型运动神经元的ＡＣｈＥ活性改变。结果表明术后１,３天实验组（指损伤给药组）和对照组（指损伤对照组）ＡＣｈＥ活性均下降（Ｐ＞００５）;术后１,２,３周对照组ＡＣｈＥ活性明显下降,而实验组ＡＣｈＥ活性逐渐趋于恢复（Ｐ＜００１）;术后６周实验组ＡＣｈＥ活性恢复至正常水平（Ｐ＜００１）。本研究显示蛇毒ＮＧＦ对坐骨神经损伤后脊髓前角运动神经元ＡＣｈＥ活性恢复有促进作用,从而对运动神经元可起一定的保护作用和促进恢复的作用     

Relation between lipid peroxidation and iron concentration in mouse liver after acute and subacute cadmium intoxication

In this study the effect of acute and subacute cadmium (Cd) intoxication on iron (Fe) concentration and lipid peroxidation (LPO) was investigated in the livers of Swiss mice. Animals were divided into two groups: the Cd group – mice intoxicated with Cd and controls. In acute time-response studies, Fe and malondialdehyde (MDA) levels were determined at 4, 6, 12, 24 and 48 h after a single oral dose of Cd (20 mg Cd/kg b.w.). In the subacute experiment, mice were given 10 mg Cd/kg b.w. orally every day for 14 days; Fe and MDA contents were determined in liver after 1 and 2 weeks. Acute Cd intoxication induced a significantly increased hepatic Fe content after 4 and 6 h, and a statistically significant increase in MDA 6, 12 and 24 h after Cd administration, although a significantly decreased MDA level was observed after 48 h. The results suggest development of early oxidative stress in livers of mice after acute intoxication with Cd. The decreased MDA observed after 48 h occurred presumably due to the adaptive response of the organism. Subacute Cd intoxication induced a significant decrease of hepatic Fe and MDA levels at both investigated time intervals compared with control. These results indicate a positive correlation between hepatic Fe and MDA content and suggest that prolonged Cd intoxication decreases hepatic LPO indirectly, by reducing the Fe content of mouse liver.     

Expression of Bcl-2, Bax and Caspase-3 in Nerve Tissues of Rats Chronically Exposed to 2,5-hexanedione

Occupational exposure and experimental intoxication with n-hexane or its metabolite 2,5-hexanedione (HD) produce a central-peripheral neuropathy. However, the mechanism remains unknown. We hypothesized that HD affected the expression of Bcl-2, Bax and Caspase-3 in the central nervous system (CNS) and the peripheral nervous system (PNS). Male adult Wistar rats were administered by intraperitoneal injection at a dosage of 200 or 400 mg/kg HD, five days per week for 8 weeks. Samples of the cerebral cortex, cerebellum, spinal cord and sciatic nerves were collected and examined for Bcl-2, Bax and Caspase-3 expression using Western blotting. Subchronic exposure to HD resulted in significantly increased expression of both anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax and Caspase-3 in cerebral cortex and cerebellum, which exhibited a dose-dependent pattern. Though little change was detected in spinal cord, our results showed that the expression of Bcl-2, Bax and Caspase-3 was markedly enhanced in the sciatic nerves. These findings suggested that the changes of apoptosis-related protein level in rat nerve tissues were associated with the intoxication of HD, which might be involved in early molecular regulatory mechanism of apoptosis in the HD-induced neuropathy.     

Neuroprotective effects of hyperbaric oxygen (HBO) therapy on neuronal death induced by sciatic nerve transection in rat

Background

Recent studies shows that hyperbaric oxygen (HBO) therapy exerts some protective effects against neural injuries. The purpose of this study was to determine the neuroprotective effects of HBO following sciatic nerve transection (SNT).

Methods

Rats were randomly divided into five groups (n?=?14 per group): Sham-operated (SH) group, SH?+?HBO group, SNT group, and SNT?+?pre- and SNT?+?post-HBO groups (100% oxygen at 2.0 atm absolute, 60 min/day for five consecutive days beginning on 1 day before and immediately after nerve transaction, respectively). Spinal cord segments of the sciatic nerve and related dorsal root ganglions (DRGs) were removed 4 weeks after nerve transection for biochemical assessment of malodialdehyde (MDA) levels in spinal cord, biochemical assessment of superoxide dismutase (SOD) and catalse (CAT) activities in spinal cord, immunohistochemistry of caspase-3, cyclooxigenase-2 (COX-2), S100beta (S100ß), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in spinal cord and DRG.

Results

The results revealed that MDA levels were significantly decreased in the SNT?+?pre-HBO group, while SOD and CAT activities were significantly increased in SNT?+?pre- and SNT?+?post-HBO treated rats. Attenuated caspase-3 and COX-2 expression, and TUNEL reaction could be significantly detected in the HBO-treated rats after nerve transection. Also, HBO significantly increased S100ß expression.

Conclusions

Based on these results, we can conclude that pre- and post-HBO therapy had neuroprotective effects against sciatic nerve transection-induced degeneration.

     

Chloroquine Intoxication Induces Ganglioside Storage in Nervous Tissue: A Chemical and Histopathological Study of Brain, Spinal Cord, Dorsal Root Ganglia, and Retina in the Miniature Pig

Abstract :
The effect of chronic chloroquine intoxication on lipid composition, particularly the gangliosides, was studied in the nervous system of miniature pigs, type Göttingen. The tissues examined were cerebrum, spinal cord, dorsal root ganglia and retina. Chloroquine was given in the diet in doses of 2.0-3.5 g/kg food. The intoxication of the pigs was started at the age of 100–240 days and continued for 177-219 days. The control pigs received the same diet without chloroquine. The ganglioside concentration was increased in all the tissues examined. Dorsal root ganglia and retina were the tissues affected most and showed a twofold increase. This corresponded to the light and electron microscopically demonstrated extensive storage process in the perikarya of dorsal root ganglion cells and inner ganglion cells of the retina. Under light microscopy the storage material was granular, intensely PAS-positive and dissolved by paraffin embedding. The electron microscopical equivalent consisted of conglomerates of membranous lysosomal residual bodies. In cerebrum the ganglioside concentration was increased by 12%. Storage in the brain varied widely between different systems and types of cells. The allocortex was much more affected than the isocortex. Certain inhibitory ganglion cell types, such as the basket cells, exhibited the most massive storage of all. The spinal medulla was morphologically less involved but showed approximately the same ganglioside increase, though not statistically significant. With the exception of cerebrum the increase in the tissues examined involved all the individual gangliosides, most severely ganglioside GM2 and three fucogangliosides. In cerebrum only the ganglioside GM2 was increased more than the other gangliosides. Chloroquine intoxication did not affect the concentration of phospholipids or cholesterol in the cerebrum, spinal cord or dorsal root ganglia, but in retina the acidic phospholipids were significantly increased.     

Effects of Chronic Restraint Stress and 17-β-Estradiol Replacement on Oxidative Stress in the Spinal Cord of Ovariectomized Female Rats

Previous studies have shown sex-specific oxidative changes in spinal cord of rats submitted to chronic stress, which may be due to gonadal hormones. Here, we assessed total radical-trapping potential (TRAP), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and lipid peroxidation (evaluated by the TBARS test) in the spinal cord of ovariectomized (OVX) female rats. Female rats were subjected to OVX, and half of the animals received estradiol replacement. Animals were subdivided into controls and chronically stressed (for 40 days). Our findings demonstrate that chronic stress decreased TRAP, and increased SOD activity in spinal cord homogenates from ovariectomized female rats and had no effect on GPx activity. On the other hand, groups receiving 17β-estradiol replacement presented a decreased GPx activity, but no alteration in TRAP and in SOD activity. No differences in the TBARS test were found in any of the groups analyzed. In conclusion, our results support the idea that chronic stress induces an imbalance between SOD and GPx activities, additionally decreasing TRAP. Estradiol replacement did not reverse the effects of chronic stress, but induced a decrease in GPx activity. Therefore, estradiol replacement in ovariectomized chronically stressed rats could make the spinal cord more susceptible to oxidative injury.     

Expression of nerve growth factor receptor mRNA is developmentally regulated and increased after axotomy in rat spinal cord motoneurons

In situ hybridization histochemistry and RNA blot analysis were used to study expression of nerve growth factor receptor (NGF-R) mRNA in rat spinal cord motoneurons. The results show that NGF-R mRNA is expressed at high levels in rat spinal cord motoneurons at the time of naturally occurring cell death. This expression is sustained, but reduced, during synapse formation and is subsequently greatly reduced in the adult spinal cord. A unilateral crush lesion of the sciatic nerve resulted in an 8-fold increase in NGF-R mRNA in adult rat spinal cord motoneurons 3 days after lesion, compared with the nonlesioned side. NGF-R mRNA induction was even more pronounced 7 and 14 days after lesion, reaching levels 12 times higher than those on the nonlesioned side. However, 6 weeks after lesion, when the motor function of the leg was largely restored, NGF-R expression had decreased to levels similar to those on the contralateral side. We therefore suggest that NGF-R mediates a trophic or axonal guidance function for developing and regenerating spinal cord motoneurons.     

Time-course of lipid peroxidation in different organs of mice treated with Echis pyramidum snake venom

This study examined the effect of Echis pyramidum (EP) venom on time-course of lipid peroxidation in different vital organs of mice. Adult male Swiss albino mice were injected with EP venom (2 mg/kg, i.p.); control mice received vehicle alone (normal saline). Mice were killed at 1, 3, 6, 12, and 24 h post-envenomation. The liver, lung, kidney, heart, and brain (cerebrum and cerebellum) were collected for the estimation of malondialdehyde (MDA), an index of lipid peroxidation. The results of this study showed that a single injection of EP venom caused a significant lipid peroxidation in all the organs studied. The onset of lipid peroxidation was as early as 1 h and persisted for several hours, suggesting an important role of oxidative stress in the cytotoxicity of EP venom.     

Effect of Garlic Supplementation on Erythrocytes Antioxidant Parameters, Lipid Peroxidation, and Atherosclerotic Plaque Formation Process in Oxidized Oil-Fed Rabbits

Effect of garlic supplementation on blood antioxidant status, lipid peroxidation, and coronary plaque formation process was investigated in oxidized oil-fed rabbits. Eighteen adult male mixed European rabbits were given a balanced diet (21 g% protein, 34 g% fat, 45 g% carbohydrate), which contained isocaloristic addition of nonoxidized or oxidized rapeseed oil in the presence and absence of garlic. The experiment lasted 24 weeks. At the beginning and every 6 weeks, rabbits were weighed, and blood was taken. To evaluate the antioxidant status of the rabbits, erythrocytes malondialdehyde (MDA) concentration, total superoxide dismutase (t-SOD), and glutathione peroxidase (GPX) activations were determined. After the experiment was completed, aortas were dissected for histological examinations. Changes in the contents of the above parameters and histological examinations showed that oxidized rapeseed, oil administered to rabbits, caused the development of atherosclerotic changes and disturbed antioxidant status. The addition of garlic in such diets inhibited atherosclerotic changes in the aorta wall, and it is related to the homeostatic activity of antioxidative enzymes and lipid peroxidation.     

Alterations of trace elements (Zn, Se, Cu, Fe) and related metalloenzymes in rabbit blood after severe trauma

To investigate the status of the trace elements (TEs) and related metalloenzymes activities in the injury and repair process after severe trauma, we established a rabbit model of severe trauma whose Injury Severity Score (ISS) was 22. Concentrations of blood selenium (Se) and serum copper (Cu), zinc (Zn), iron (Fe), and ferritin were measured on D0 (before injury), and day (D) 1, D2, D3, D6, D9, D14, D21, D28 after trauma, respectively. The activities of glutathione peroxidase (GPx), Cu/Zn superoxide dismutase (Cu/Zn-SOD), myeloperoxidase (MPO), the contents of lipid peroxidation product malondialdehyde (MDA) and serum biochemical profile were detected synchronously. In addition, the morphologic changes of major organs were observed at different time intervals. Results showed that blood Se and serum Zn, Fe contents decreased significantly within 2 weeks after injury. Serum Cu concentration was significantly reduced on D1 but normalized quickly. Serum ferritin level increased during the first week while following an obvious decrease thereafter. The blood GPx activity dropped markedly from D1 to D6, the serum Cu/Zn-SOD activity decreased on D1 and then increased significantly within 2 weeks, and the blood MPO-positive stained cells increased within a week after trauma and followed by a decrease from D14 to D21. The serum MDA increased significantly on D6. Seven of 34 rabbits died in 4-6 days after injury. Biochemistry values and pathological features revealed these rabbits died of multiple organ dysfunction syndrome (MODS). Our experiment suggested that the circulating TEs status is dramatically modified in response to trauma, which might be a factor in MODS.     

Ontogenic characteristics of lipid peroxidation and antioxidant system enzymes in the brain of geese

Peculiarities of antioxidant homeostasis of geese brain tissue during embryogenesis and early postnatal period have been studied. It has been shown that the cerebrum and hindbrain tissues are characterized by a higher level of lipid peroxidation compared to liver. Main antioxidative enzymes' activity (superoxide dismutase, catalase, glutathione peroxidase) in the brain already reaches its maximum in the middle period of embryogenesis. We have found that brain tissues are characterized by a lower activity of intracellular enzymes (superoxide dismutase, catalase) but increased glutathione peroxidase activity as compared to liver. The rate of Fe2+ initialized lipid peroxidation and coefficient of antioxidative activity were used as a criterion for evaluation of antioxidative system's status. According to the dynamics of these factors the highest tension of antioxidative system in the brain appears in the period of the contour (28 days) and juvenile (49 days) feather formation.