Static magnetic field expose enhances neurotransmission in crayfish nervous system.

PURPOSE: To investigate the effects of static magnetic field (SMF) exposure on the synaptic transmission in a tail-flip circuit of crayfish. MATERIALS AND METHODS: An O-shaped permanent magnet (35 mT intensity) was placed under the isolated nerve cord of crayfish to provide static magnetic field exposure. Using electrophysiological methods, the excitatory post synaptic potential (EPSP) before and after field exposure in the lateral giant interneuron were measured and compared. RESULTS: The EPSP produced via electrical and chemical synapses in the lateral giant neuron were enhanced after 30 min of SMF exposure (8.08 mT). Perfusion of field-exposed crayfish bath solution or preloading of Ca(2+) chelator and intracellular Ca(2+) release blocker failed to observe the SMF-induced enhancement on EPSP. CONCLUSIONS: Exposure of SMF increases the efficacy of synaptic-transmission in crayfish tail-flip escape circuit and this SMF-induced potentiation is a Ca(2+) dependent phenomenon.

Prevalence and risk factors associated with dyslipidaemia in children and adolescents among ethnic groups in Taiwan.

BACKGROUND: The mortality rates of cerebral and cardiovascular diseases are higher for aborigines than non-aborigines in Taiwan. Hypertriglyceridaemia and hypercholestolaemia are risk factors for cardiovascular diseases. OBJECTIVES: To investigate the prevalence of dyslipidaemia and its associated risk factors in aborigine (Atayal, Paiwan and Bunun tribes) and non-aborigine (Fukein and Hakka Chinese) children and adolescents in Taiwan. STUDY DESIGN: This was a cross-sectional study. METHODS: In total, 718 males and 721 females, below 20 years of age, were recruited. Our study defined dyslipidaemia as serum triglyceride and cholesterol levels greater than 200 and 240 mg/dl, respectively. RESULTS: The serum triglyceride level and the prevalence of hypertriglyceridaemia were similar in both aborigines and non-aborigines and both sexes, but the Bunun and Paiwan tribes had the highest prevalence of hypertriglyceridaemia in males (11.8-29.4%) and females (10.9-22.8%) compared with other aboriginal tribes (5.1-10.8% for males and 7.8-9.2% for females). Serum cholesterol concentrations and the prevalence of hypercholesterolaemia were lower in the aborigines than non-aborigines for both sexes (P<0.05), with the Atayal tribe having the lowest prevalence in males (1.1%) and females (2.1%) compared with other aboriginal tribes (2.4-4.5% for males and 5.7-8.0% for females). Using multivariate-adjusted logistic regression modelling, hypertriglyceridaemia was significantly associated with the Bunun tribe (odds ratio (OR)=3.2, 95% confidence intervals (CI) 1.6-6.1), hyperuricaemia (OR=1.8, 95% CI 1.2-2.6), hypercholesterolaemia (OR=3.3, 95% CI 1.7-6.4) and alcohol use (OR=2.8, 95% CI 1.2-6.6). Hypercholesterolaemia, after controlling for age and sex, was significantly associated with the Atayal tribe (OR=0.2, 95% CI 0.1-0.5), hypertriglyceridaemia (OR=3.5, 95% CI 1.8-6.7) and hyperuricaemia (OR=3.2, 95% CI=1.7-6.0). CONCLUSIONS: For the young people of Taiwan, hypertriglyceridaemia is associated with hyperuricaemia, hypercholesterolaemia and alcohol use, and hypercholesterolaemia is associated with hypertriglyceridaemia and hyperuricaemia. Compared with non-aborigines, the young aborigines of some tribes have a higher prevalence of hypertriglyceridaemia and a lower serum cholesterol level.

Long-lasting potentiation of excitatory synaptic signaling to the crayfish lateral giant neuron.

The neural circuit that underlies the lateral giant fiber (LG)-mediated reflex escape in crayfish has provided findings relating synaptic change to nonassociative learning such as sensitization and habituation. The LGs receive sensory inputs from the primary sensory afferents and a group of mechanosensory interneurons (MSIs). An increase of excitability by suprathreshold repetitive excitation of this circuit, which is similar to Hebbian long-term potentiation (LTP), has been reported. This potentiation was previously thought to result from the enhancement of transmission at cholinergic synapses between primary afferents and MSIs but not the electrical synapses onto LG. In this study, we found that potentiation of synaptic signaling at the electrical synapse onto LG can also be induced when the synapse was activated with subthreshold repetitive pulses or with a few strong suprathreshold shocks. LG LTP was induced in the preparation which had received pulses at limited frequency range. Although whether this LTP is involved in the learning process of escape behavior in crayfish is not clear, the intensity and amount of sensory stimulation used here mimicked those that could easily be produced by a predator trying to catch a crayfish and could be of adaptive significance in life.

Diode-pumped passively Q-switched picosecond Nd:GDxY1-xVO4 self-stimulated raman laser.

An efficiency of 8.2% is demonstrated for a diode-pumped passively Q-switched self-stimulated Raman laser with an a-cut mixed vanadate crystal, Nd:Gd0.8Y0.2VO4. At 2.2 W of incident pump power, the self-stimulated Raman laser produces pulses as short as 660 ps at a Stokes wavelength of 1175 nm with 2.7 microJ of energy per pulse at a 66-kHz repetition rate.

Free radical-triggered hepatic injury of experimental obstructive jaundice of rats involves overproduction of proinflammatory cytokines and enhanced activation of nuclear factor kappaB.

Excessive production of hydroxyl radicals in blood and liver has previously been demonstrated by us in rats with obstructive jaundice induced by common bile duct ligation (CBDL). In this study, we demonstrate overproduction of superoxide radicals in circulating blood of CBDL rats by the lucigenin-amplified chemiluminescence technique. To pinpoint the molecular agents that mediate these processes, we measured circulating proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta ( IL-1beta), and interleukin-6 (IL-6) in controls and CBDL rats. Concentrations of these cytokines in blood of CBDL rats were markedly elevated when compared to the controls (TNF-alpha: 36.7 +/- 5.0 vs 13.8 +/- 0.5 pg/mL; IL-6: 2,814 +/- 1,740 vs 0 pg/mL; IL-1beta: 11.9 +/- 2.6 vs 0 pg/mL). The overproduction of free radicals triggered by elevated cytokines in CBDL rats was correlated with the activation of NF-kappaB in hepatic tissue. Using the TdT-mediated dUTP nick-end label staining technique, we showed that hepatic tissue sections from CBDL rats had an increase in the apoptotic index (AI). Based on these findings, we propose that the severe hepatic injury in CBDL rats is mediated by a cycle that involves the activation of NF-kappaB by combined action of proinflammatory cytokines and reactive oxygen species (ROS). NF-KB, in turn, initiates the transcription of cytokine genes (eg, IL-6, IL-8, TNF-alpha), which triggers hepatic injury, at least in part, by a free radical-mediated apoptotic mechanism. Elevated ROS may be as a positive-feedback signal that triggers NF-KB reactivation; the severe hepatic injury of CBDL rats may result from perpetuation of this vicious cycle.

Antimutagenicity of extracts of Hericium erinaceus.

Hericium erinaceus is valuable in the diet and in medical treatment. It contains water-soluble polysaccharides that have been found to enhance immunity and which show anti-artificial pulmonary metastatic tumor effects. In this study, water and ethanol extracts of the mycelium and fruiting body of Hericium erinaceus were examined by the Ames test using Salmonella typhimurium TA98 to screen for antimutagenic effects against 5 mutagens: AFB1, B[a]P, Glu-P-1, NQNO, and Trp-P-1. We found that both extracts have the strongest antimutagenic activity against Trp-P-1, followed by Glu-P-1, B[a]P-1, AFB1, and finally NQNO. In addition, the antimutagenicity of the extracts was produced in a concentration-dependent manner. At a concentration of 200 ppm, both extracts showed the highest inhibitory action. However, the linear correlation indicated that concentration-activity relationship was not significant (p > 0.05). In addition, extracts showed less antimutagenicity after heat treatment (p < 0.05). This suggests that the antimutagenicity of the extracts is heat-labile. The ethanol extract from mycelium or fruiting body had better antimutagenic effects than did the water extract (p < 0.05). Also, the extract from the fruiting body had better antimutagenic effects than did that from the mycelium.

Functional blocking of integrin-associated protein impairs memory retention and decreases glutamate release from the hippocampus.

We have previously demonstrated that integrin-associated protein is involved in memory consolidation of one-way inhibitory avoidance learning in rats and mice. In the present study, we examined the effects of functional blocking of integrin-associated protein on memory retention, long-term potentiation and glutamate release in mice as well as on cell attachment to extracellular matrix protein in primary cultures. The results indicated that integrin-associated protein monoclonal antibody miap301, when directly injected into the dentate gyrus of the hippocampus at moderate doses, significantly impairs memory retention in mice in the same one-way inhibitory avoidance task and decreases the amplitude of tetanic stimulation-induced long-term potentiation in dentate gyrus neurons. At a dose that effectively impairs both memory retention and long-term potentiation, integrin-associated protein monoclonal antibody also significantly blocks potassium chloride-induced glutamate release from the hippocampus in vivo. Results from western blot confirmed the presence of integrin-associated protein at the synaptic area. Cell adhesion experiments further revealed that integrin-associated protein monoclonal antibody markedly inhibits granular cell attachment to thrombospondin, the extracellular matrix protein known to bind integrin-associated protein, but not to collagen and laminin, the extracellular matrix proteins known to bind integrin. From these results we suggest that integrin-associated protein monoclonal antibody may impair synaptic plasticity and behavioral plasticity in mice through blockade of granular cell attachment to extracellular matrix protein and the subsequent signal transduction, and through inhibition of glutamate release from the hippocampus.

Effects of S-adenosyl-L-methionine on liver damage in experimental obstructive jaundice.

S-adenosyl-l-methionine (SAMe) is a naturally occurring molecule distributed throughout the body tissues, including the liver. It acts as a methyl group donor and as an enzyme activator in a number of biochemical reactions. Methionine is metabolized in the liver, where it is converted to SAMe by SAMe-synthetase. In patients with liver diseases, these pathways are impaired because of the decreased contents of glutathione, the major abnormality being a reduction in SAMe-synthetase activity. Exogenous SAMe may overcome the results of impaired SAMe-synthetase activities. We conducted this study to evaluate the effect of SAMe administration on liver damage induced by biliary obstruction. Rats with common bile duct ligation exhibited abnormal liver functions, increased lipid peroxide levels, and decreased reduced glutathione contents when compared with the shammed-controls, which indicated that there was oxidative stress in rats with obstructive jaundice; however, SAMe application improved these injuries. There were significant alterations of the levels of amino acid profiles in animals with obstructive jaundice. The ratio between branch chain and aromatic amino acid was depressed, which indicated that the condition of liver was worsening, but SAMe administration improved these alterations significantly. In conclusion, SAMe administration alleviated the liver damage, indicating an important hepatoprotective effect of this methyl donor.

Corticotropin-releasing factor produces a protein synthesis--dependent long-lasting potentiation in dentate gyrus neurons.

Corticotropin-releasing factor (CRF) was shown to produce a long-lasting potentiation of synaptic efficacy in dentate gyrus neurons of the rat hippocampus in vivo. This potentiation was shown to share some similarities with tetanization-induced long-term potentiation (LTP). In the present study, we further examined the mechanism underlying CRF-induced long-lasting potentiation in rat hippocampus in vivo. Results indicated that the RNA synthesis inhibitor actinomycin-D, at a concentration that did not change basal synaptic transmission alone (5 microgram), significantly decreased CRF-induced potentiation. Similarly, the protein synthesis inhibitor emetine, at a concentration that did not affect hippocampal synaptic transmission alone (5 microgram), also markedly inhibited CRF-induced potentiation. These results suggest that like the late phase of LTP, CRF-induced long-lasting potentiation also critically depend on protein synthesis. Further, prior maximum excitation of dentate gyrus neurons with tetanization occluded further potentiation of these neurons produced by CRF and vise versa. Moreover, quantitative reverse transcription-polymerase chain reaction analysis revealed that CRF mRNA level in the dentate gyrus was significantly increased 1 h after LTP recording. Together with our previous findings that CRF antagonist dose-dependently diminishes tetanization-induced LTP, these results suggest that both CRF-induced long-lasting potentiation and tetanization-induced LTP require protein synthesis and that CRF neurons are possibly involved in the neural circuits underlying LTP.

Psychopharmacology in autism.

Autism is a neurobiological disorder. The core clinical features of autism include impairment in social interaction, impairments in verbal and nonverbal communication, and restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. Autism often has coexisting neuropsychiatric disorders, including seizure disorders, attention deficit hyperactivity disorder, affective disorders, anxiety disorder, obsessive-compulsive disorder, and Tourette disorder. No etiology-based treatment modality has been developed to cure individuals with autism. However, comprehensive intervention, including parental counseling, behavior modification, special education in a highly structured environment, sensory integration training, speech therapy, social skill training, and medication, has demonstrated significant treatment effects in many individuals with autism. Findings from preliminary studies of major neurotransmitters and other neurochemical agents strongly suggest that neurochemical factors play a major role in autism. The findings also provide the rationale for psychopharmacotherapy in individuals with autism. This article reviews studies of neurochemical systems and related psychopharmacological research in autism and related neuropsychiatric disorders. Clinical indications for pharmacotherapy are described, and uses of various medications are suggested. This article also discusses new avenues of investigation that may lead to the development of more effective medication treatments in persons with autism.

Biochemical markers for assessment of bone metastases in patients with breast cancer.

Breast cancer commonly metastasizes to bones, producing both osteolytic and osteoblastic deposits. Different markers for quantitative determination of bone turnover have been developed to evaluate bone metastases of breast cancer. The urinary deoxypyridinoline (Dpd), a crosslink product of collagen molecules found in bone and excreted in urine during bone degradation, and bone specific alkaline phosphatase (B-ALP), an isoenzyme localized in the membrane of osteoblasts and released in circulation during bone formation, were recently described as a group of markers of bone turnover in metastatic cancer. The urinary Dpd/creatinine (Cre) ratios and the serum B-ALP activity were determined in the samples from 148 patients who suffered from breast cancer (BC patients) with or without bone metastases, and 42 healthy women. For comparison, other biochemical markers, e.g. carcinoembryonic antigen (CEA), CA15-3, tissue polypeptide antigen (TPA), tissue polypeptide specific antigen (TPSA), and total alkaline phosphatase (T-ALP) in these samples were also evaluated. The results showed that there was a significant difference in urinary Dpd/Cre ratio between the control group and the patients with breast cancer (BC group) (mean +/- S.D., 5.69 +/- 1.26 vs. 8.19 +/- 3.95 nM/mM, P < 0.05). However, there was no significant difference between their B-ALP activities in the two groups. In addition, the BC patients with bone metastases showed elevated urinary Dpd/Cre ratios and B-ALP activities and ratios of (Dpd/Cre)/B-ALP in compare with BC patients without bone metastases (P < 0.05). Meanwhile, the urinary Dpd/Cre ratios (10.50 +/- 5.04 nmol/mmol) in the advanced stage of BC patients were higher than those in an early stage (7.45 +/- 3.23 nmol/mmol) (P < 0.05), but their serum B-ALP activities increased only in stage IV (P < 0.05). The urinary Dpd/Cre ratios also increased progressively according to the degree of bone metastases (P < 0.05), but their serum B-ALP activities only increased in severe bone metastases (P < 0.05). The results showed that the increase of a bone osteolytic activity took place earlier than that of a bone osteoblastic activity in the metastatic BC patients. In compare with other conventional markers, the best diagnostic efficiency of biochemical markers, analyzed by step wise discriminate analysis, was provided by CEA followed by Dpd/Cre ratio, CA15-3, TPA, TPSA, B-ALP and T-ALP. We conclude that showed the urinary Dpd/Cre ratio was a useful tumor marker to evaluate breast cancer with bone metastases.

Insertion of atToc34 into the chloroplastic outer membrane is assisted by at least two proteinaceous components in the import system.

Toc34 is a member of the outer membrane translocon complex that mediates the initial stage of protein import into chloroplasts. Toc34, like most outer membrane proteins, is synthesized in the cytosol at its mature size without a cleavable transit peptide. The majority of outer membrane proteins do not require thermolysin-sensitive components on the chloroplastic surface or ATP for their insertion into the outer membrane. However, different results have been obtained concerning the factors required for Toc34 insertion into the outer membrane. Using an Arabidopsis homologue of pea Toc34, atToc34, we show that the insertion of atToc34 was greatly reduced by thermolysin pretreatment of chloroplasts as assayed either by protease digestion or by alkaline extraction. The insertion was also dependent on the presence of ATP or GTP. A mutant of atToc34 with the GTP-binding domain deleted still required ATP for optimal insertion, indicating that ATP was used by other protein components in the import system. The ATP-supported insertion was observed even in thermolysin-pretreated chloroplasts, suggesting that the protein component responsible for ATP-stimulated insertion is a different protein from the thermolysin-sensitive component that assists atToc34 insertion.

Comparison of serum copper, magnesium, zinc and calcium levels between G6PD deficient and normal Chinese adults.

Minerals are important for normal hematopoiesis and may play a role in acute hemolytic anemia induced by G6PD deficiency. To compare serum magnesium, copper, zinc and calcium levels between G6PD deficiency and normal control adults, we investigated 69 G6PD deficient (28 male, 41 female) and 61 age- matched G6PD normal adults (26 male, 35 female). Serum magnesium, copper, zinc and calcium levels were determined by atomic absorbance spectrometry. Our results revealed that male adults with G6PD deficiency had significantly higher serum copper and magnesium levels than those of the control group (P < 0.01, < 0.05, respectively). In G6PD normal adults, serum copper levels were significantly lower in males than in females (P < 0.01). In the group of G6PD deficiency adults, serum copper levels in males (103.0 +/- 10.4 ug/dL) were significantly lower than those in females (139.0 +/- 34.3 ug/dL) (P < 0.01). Serum magnesium values and zinc values in males (2.42 +/- 0.38 mEq/L and 102.2 +/- 26.5 ug/dL) were significantly higher than those in females (2.07 +/- 0.20 mEq/L and 87.0 +/- 14.9 ug/dL) (P all < 0.01). Female adults with G6PD deficiency had significantly higher serum calcium levels and lower magnesium levels than those of the control group (P all < 0.01). The significantly higher levels of serum copper and magnesium in G6PD deficient male adults may play some role concerning red blood cells in resistance to plasmodium falciparum.

Serum vitamin A level in breast cancer patients.

Vitamin A or its synthetic analogues are potent in controlling cell differentiation and in preventing epithelial cancer in experimental animals. Although some community-based studies have found that high serum retinol levels in prediagnostic sera were associated with reduced risk for cancer, other reports in humans have not confirmed this finding. This study is to evaluate the preoperative serum vitamin A level in breast cancer patients in Taiwan. The serum specimens were collected from 106 female cases of breast cancer (aged 30 to 70 years), 32 female cases of benign breast disease (aged 29 to 57 years), and 40 healthy females (aged 22 to 52 years). The serum vitamin A levels were measured by colorimetic analysis. The results showed the mean value of the vitamin A level was 140.4 +/- 65.7 micrograms/dl in the breast cancer group comparing to 145.2 +/- 44.2 micrograms/dl in the benign breast disease group, 144.0 +/- 30.0 micrograms/dl in the control group (P > 0.05). The characteristics of the breast cancer group were analyzed and they revealed that serum vitamin A levels did not bear statistically significant differences in age, duration, steroid receptor, tumor size and menopausal state. (P > 0.05) In conclusion, the serum vitamin A levels were not decreased in early breast cancer patients. The serum vitamin A levels were significantly decreased in the metastatic breast cancer group, especially in liver metastatic women. (P < 0.05). Postoperative vitamin A supplement may have potential benefit to metastatic breast cancer patients.

Evidence for accelerated generation of hydroxyl radicals in experimental obstructive jaundice of rats.

We present evidence herein of the accelerated generation of hydroxyl radical (.OH) in the plasma and the liver tissue of common bile duct ligated (CBDL) rats, a model for experimental obstructive jaundice. .OH production in the plasma was monitored in vivo by the identification of dihydroxybenzoates in plasma [2,3-dihydroxybenzoate (2,3-DHB) and 2,5-dihydroxybenzoate (2,5-DHB)] using high performance liquid chromatography (HPLC). The average concentrations of 2,3-DHB and 2,5-DHB produced in the plasma of the controls were 33+/-3 microM and 232+/-34 microM (n = 15), respectively, whereas their respective concentrations increased to 149+/-28 microM and 604+/-88 microM in the CBDL rats (n = 19). Furthermore, we also observed a time-dependent decreasing trend of 2,3-DHB and 2,5-DHB production after surgical removal of the ligation of the experimental animals. In addition, the generation of .OH in the liver tissue was studied by using dimethyl sulfoxide (DMSO) as a molecular probe and measuring the amount of methanesulfinic acid (MSA), the product of the trapping reaction. The net production of MSA in the liver tissue of the control rats was 1.22+/-0.05 O.D. unit/g protein (n = 5), whereas its respective concentration of MSA in the liver tissue of CBDL rats increased to 2.05+/-0.15 O.D. unit/g protein (n = 5). In addition, we showed that CBDL rats receiving a pretreatment of mannitol, an .OH scavenger, resulted in the decreased production of MSA. Electron micrographic study indicated that the most prominent change observed in CBDL rats was the alteration of mitochondria, which were swollen with distorted cristae. Meanwhile, the bile canaliculi were moderately more dilated than that of the controls, and an increased neutrophil peripheral blood count was found in CBDL rats when compared to the controls. Taken together, our data suggest that accelerated generation of .OH in the CBDL rats is obvious and may play a key role in the pathogenesis of liver damage associated with obstructive jaundice.

Effect of vitamin E, topical hypothermia and steroid on ischemic liver in rats.

Major hepatic surgery often requires temporary occlusion of the porta hepatis in order to minimize intraoperative bleeding. Occlusion of porta hepatis induces hepatic ischemia and may cause liver damage. This study was conducted to evaluate the effects of vitamin E, topical hypothermia and administration of steroids on ischemic liver by assessing the hepatic levels of lipid peroxides and examining the ultrastructural change of mitochondria. One hundred and twenty male wistar rats were divided into four groups, each of 30. All rats underwent laparotomy and the liver ischemia experiment was conducted by clamping the porta hepatis for 15 minutes. Group A received no further treatment, group B received vitamin E (30IU/Kg/B.W) supplementation for one week before experiment, group C was topically cooled and group D received preocclusion intravenous methylprednisolone (2mg/Kg/B.W). Hepatic lipid peroxides, expressed as nmol MDA/g wet wt were assessed by spectrofluorometric methods, and were measured immediately before occlusion, 15 min after occlusion, and 15 min after reperfusion. The results showed that the concentration of lipid peroxides increased markedly after occlusion of porta hepatis in group A, which received no treatment in ischemic liver (8.76 +/- 3.19 vs. 10.49 +/- 3.35 MDA nmol/g wet wt, p < 0.05, paired t-test), while the concentrations of hepatic lipid peroxides were not found to increase in groups B, C or D. In the meantime, the ultrastructural study showed marked swelling of mitochondria in ischemic liver of group A rats only. This suggests that vitamin E supplementation, topical hypothermia and administration of steroids will inhibit the propagation of lipid, peroxidation and provide protective effects on liver parenchyma during ischemia.

Biochemical events associated with ligation of the common bile duct in Wistar rats.

Oxygen free radicals have been implicated as mediators of tissue injury in a variety of diseases. We investigated the role of oxidative injury and oxygen free radical scavengers in liver cell injury associated with obstructive jaundice in Wistar rats. Bile duct ligation for 4 or 7 days led to a decrease in both vitamin E and A in the plasma and liver of male Wistar rats, indicating the malabsorption of lipid-soluble vitamins. Serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase activities were increased in the bile-duct-ligated rats. Furthermore, marked increases in lipid peroxide and oxidized glutathione levels indicated cholestatic liver injury. The antioxidant defense system was impaired, as shown by decreases in reduced glutathione and in the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase. Moreover, these high lipid peroxide levels and low levels of antioxidants correlated with the severity of jaundice. After releasing the bile duct ligation, levels of bilirubin, lipid peroxide and oxidized glutathione declined, while the levels of vitamin E and A, reduced glutathione, and the activities of GSH-Px increased, indicating an improvement in liver function. These findings suggest that lipid peroxidation is associated with the pathogenesis of liver damage in animals with bile duct ligation. Meanwhile, free oxygen radical scavengers are reduced in the bile-duct-ligated rats, thereby increasing the susceptibility of the liver to injury by oxygen-derived free radicals.

Synthesis of Hsp72 induced by exercise in high temperature.

An investigation was undertaken involving the physiological effects of exercise in high temperature and its effect on the induction of heat shock proteins synthesis in peripheral lymphocytes and gastrocnemius. Male Long-Evans rats were employed. Environmental temperature was designed as three conditions: room temperature (26-27 degrees C), middle temperature (30-31 degrees C), and high temperature (36-37 degrees C). Rats were divided into one of three groups and exercised passively in an automatic round treadmill. Body temperature, biochemical changes were determined and the synthesis of heat shock protein 72 were analyzed by SDS-PAGE and immunochemical stain with monoclonal anti-Hsp72 antibody. Those results indicated that the body temperature elevated faster and higher in rats of high-temperature exercise group than those of a house temperature significantly (p < 0.05). Hsp72 could be detected only in lymphocytes from rats exercising in high temperature more than 60 minutes whose body temperatures were elevated above 41 degrees C. The induced Hsp72 appeared in lymphocytes 2 hours after exercise and reached maximally at 16-24 hours and then disappeared gradually. In gastrocnemius, Hsp72 could be detected even before the passive exercise, and its amount changed as in lymphocytes did in all three groups. No difference was found in blood sugar, hematocrit and CK among the three groups of rats. On the basis of above results, we can conclude that Hsp72 is synthesized in the muscle of intact rats, and exercise is a sufficient inducer. For lymphocytes, the presence of Hsp72 can be viewed as a heat stress in exercise.