OBJECTIVETo explore the relationship between the expression of heat shock protein 90, 60 and 27 (HSP90, HSP60 and HSP27) and genetic damage in peripheral blood of workers exposed to coke oven emissions.

METHODS288 coke oven workers in a steel factory were divided into the high-dose group and the low-dose group on the basis of environment monitoring result and work place. There were 172 men in high-dose group (workers who worked at the oven top and oven side) and 116 men in low-dose group (workers who worked at the oven bottom and others who were engaged to aided work). 38 workers unexposed occupationally to carcinogenic substances were selected as the control group, who were employed in medical therapy unit nearby 2 kilometers from the steel factory. Their general information, history of personal and occupational exposure, and the work environment were investigated. Blood samples were collected immediately after a shift at the end of a working day from 288 coke oven workers and 38 control workers. Levels of HSP90, HSP60 and HSP27 in peripheral blood lymphocytes were measured by Western blot, and the degree of DNA damage was detected by the comet assay.

RESULTSLevels of HSP90 in peripheral blood lymphocytes in three groups were 0.24 +/- 0.32, 0.12 +/- 0.30 and 0.06 +/- 0.33 respectively. They increased significantly compared with that of the control. But levels of HSP60 and HSP27 were not significantly different among those groups. Compared with the control group, there was significant difference in tail length, olive tail moment et al of SCGE (G +/- s(G)) of occupational exposure workers. High-dose group > low-dose group > control group (P < 0.05). The degree of DNA damage increased with the rise of exposure BaP dose (Spearman r = -0.345, P < 0.01).

CONCLUSIONLevels of HSP90 in peripheral blood lymphocytes and the degree of DNA damage increase with the rise of exposure polycyclic aromatic hydrocarbons (PAHs) dose.

Adult ; Chaperonin 60 ; blood ; Coke ; adverse effects ; Comet Assay ; DNA Damage ; drug effects ; HSP27 Heat-Shock Proteins ; blood ; HSP90 Heat-Shock Proteins ; blood ; Humans ; Lymphocytes ; metabolism ; Male ; Occupational Exposure ; adverse effects ; Polycyclic Aromatic Hydrocarbons ; adverse effects

Heat contact urticaria is very rare and it is characterized by the development of wheal limited to the areas of heat contact. We report a case of heat contact urticaria in a 65-year-old women. The wheal was induced by hot bathing, washing in hot water or leaning on hot radiators. Symptoms started within 5 minutes of exposure and lasted 30 to 60 minutes. She had no systemic symptoms. The clinical diagnosis of localized heat urticaria was confirmed by experimental induction of localized wheals. Our investigation showed that the threshold temperature needed for induction of the heat urticaria was 39 degrees C. We tried to investigate the plasma levels of prostaglandin D2 and blood histamine before and after heat challenge. The patient showed marked improvement after a combination treatment of desensitizing by repeated exposure to heat and indomethacine.
Aged ; Case Report ; Female ; Heat/*adverse effects ; Human ; Prostaglandin D2/blood ; Urticaria/*etiology/therapy

OBJECTIVETo study the change of heat shock protein (HSP)70 expression after exposure to occupational microwave in rats hippocampus, and explore the role of HSP70 in the mechanism of bio-effect of microwave irradiation.

METHODSThe animal model was established by whole body exposures in 90, 5 W/cm(2) microwave irradiation field for 20 min in rats. Changes of the mRNA of hsp70 expressions in rat hippocampus at different time were studied by RT-PCR, and the protein change by Western blot.

RESULTSThe mRNA and protein expression of hsp70 in rat hippocampus increased after 90 W/cm(2) and 5 W/cm(2) microwave irradiation for 20 min. The anal temperature and the value of SAR increased significantly. These changes were positively correlated with power and irradiation time of microwave. The results indicated that microwave irradiation led to HSP70 syntheses effectively.

CONCLUSIONMicrowave irradiation can obviously induce the thermal effect and activate HSP70, and initiate the endogenous protective mechanism of central nervous system.

Animals ; HSP70 Heat-Shock Proteins ; genetics ; metabolism ; Hippocampus ; metabolism ; radiation effects ; Microwaves ; adverse effects ; RNA, Messenger ; genetics ; Rats ; Rats, Wistar

OBJECTIVEThe present study was designed to investigate the effects of subchronic low level microwave radiation (MWR) on cognitive function, heat shock protein 70 (HSP70) level and DNA damage in brain of Fischer rats.

METHODSExperiments were performed on male Fischer rats exposed to microwave radiation for 90 days at three different frequencies: 900, 1800, and 2450 MHz. Animals were divided into 4 groups: Group I: Sham exposed, Group II: animals exposed to microwave radiation at 900 MHz and specific absorption rate (SAR) 5.953 × 10-4 W/kg, Group III: animals exposed to 1800 MHz at SAR 5.835 × 10-4 W/kg and Group IV: animals exposed to 2450 MHz at SAR 6.672 × 10-4 W/kg. All the animals were tested for cognitive function using elevated plus maze and Morris water maze at the end of the exposure period and subsequently sacrificed to collect brain tissues. HSP70 levels were estimated by ELISA and DNA damage was assessed using alkaline comet assay.

RESULTSMicrowave exposure at 900-2450 MHz with SAR values as mentioned above lead to decline in cognitive function, increase in HSP70 level and DNA damage in brain.

CONCLUSIONThe results of the present study suggest that low level microwave exposure at frequencies 900, 1800, and 2450 MHz may lead to hazardous effects on brain.

Animals ; Cognition ; radiation effects ; DNA Damage ; HSP70 Heat-Shock Proteins ; genetics ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Inbred F344

OBJECTIVETo investigate the effects of microwave irradiation on the expression and regulation of heat shock proteins (HSPs) in primary cultured rat hippocampal neurons.

METHODSNeurons were exposed to 90 mW/cm(2) microwave irradiation for 10 minutes. Western blot was used to determine the expression of HSP27, HSP70, HSP90 and heat shock factor 1 (HSF1) at 0, 3, 6, 12 and 24 hour respectively. Real-time RT-PCR was used to determine the mRNA expression of HSF1. DNA-binding activity of HSF1 was measured by electrophoretic mobility shift assay (EMSA).

RESULTSThe protein expression of HSP27 was significantly increased by 22%, 36%, 18% at 3, 6, 12 h, respectively (P < 0.05). The protein expression of HSP70 was significantly increased by 23%, 32%, 26% at 3, 6, 12 h, respectively (P < 0.05, P < 0.01). The protein expression of HSP90 was significantly increased by 27%, 33% at 6, 12 h, respectively (P < 0.05, P < 0.01). The DNA-binding activity of HSF1 was stimulated, however, no significant change of the expression of HSF1 was observed on both the mRNA and protein levels.

CONCLUSIONThe transcriptional activity of HSF1 is activated by microwave irradiation, which promotes the expression of HSPs. Heat shock response which contributes to establish a cytoprotective state is induced by microwave irradiation in primary cultured rat hippocampal neurons.

Animals ; Cells, Cultured ; Heat-Shock Proteins ; metabolism ; Hippocampus ; metabolism ; radiation effects ; Microwaves ; adverse effects ; Neurons ; metabolism ; Rats

OBJECTIVETo investigate the relationship between heat shock protein 72 (Hsp72) and DNA genetic damage in peripheral blood lymphocytes of coke oven workers and the role of Hsp72 in protection of cells from genetic damage induced by coke oven emissions.

METHODSTwo hundred and sixty-seven coke oven workers and thirty controls without occupational PAHs exposure were investigated. Benzo[a]pyrene concentrations in the ambient air individually collected were assayed by high performance liquid chromatography (HPLC). Western Blot was used to measure Hsp72 levels and Comet assay was used to evaluate DNA damage degree. Personal information was collected by questionnaire.

RESULTSThe Hsp72 level (G+/-S(G)) and olive comet tail moment (G+/-S(G) of peripheral blood lymphocytes in high-exposure workers (1.24 +/- 0.42 and 4.49 +/- 1.24) were significantly higher than those in low-exposure workers (1.01 +/- 0.35 and 2.99 +/- 1.10, P < 0.05) and control (0.85 +/- 0.34 and 2.40 +/- 1.00, P < 0.05) respectively. The Hsp72 median level of all subjects was used as the limit to divide subjects into high Hsp72 level group and low Hsp72 level group. The rate with high Hsp72 level was 36.7%, 43.1% and 58.3% in control, low exposure and high exposure workers respectively and had a rising tendency following exposure level (P = 0.003). In high Hsp72 level group Hsp72 level in high exposure workers was significantly higher than that in control (P < 0.05), and there was a rising tendency along with the increase of exposed levels. But the olive comet tail moment had no significant difference among three exposed groups (P > 0.05). In low Hsp72 level group there no difference among three exposed groups about Hsp72 levels. The olive comet tail moment in high exposure workers was significantly higher than that in low exposure workers and control (P < 0.01) and high exposure workers in Hsp72 positive group and there was a rising tendency along with the increase of exposed levels. Hsp72 levels had strong negative correlation with the olive comet tail moment (r = -0.503, P < 0.01) in high exposure workers.

CONCLUSIONThe coke oven emissions can induce hsp72 expression. Hsp72 play a role of protecting cells from DNA damage induced by coke oven emissions.

Adult ; Benzo(a)pyrene ; adverse effects ; Coke ; DNA Damage ; HSP72 Heat-Shock Proteins ; blood ; Humans ; Lymphocytes ; metabolism ; Male ; Occupational Exposure ; adverse effects

10 male subjects participated in the environmental simulation study to evaluate the operation ergonomics at high-temperature in the cockpit. Grip strength, perception, dexterity, reaction and intelligence were measured respectively during the tests at 40 degrees C and 45 degrees C, simulating the high-temperatures in a simulation cockpit chamber. Then the data obtained were compared to the combined index of heat stress (CIHS). The average values of each item of the subjects' performance at the two different temperatures are compared. The results indicated that CIHS exceeded the heat stress safety line after 45 min at 40 degrees C, grip strength decreased by 12%, and perception increased by 2.89 times. In contrast, at 45 degrees C, CIHS exceeded the safety line after 20 min, grip strength decreased by 3.2%, and perception increased by 4.36 times. However, Finger dexterity was less affected. Reaction ability was first accelerated, and then slowed down. The error rate in the intelligence test increased to a greater extent. At the high temperatures, the minimum perception was the most affected, followed by grip strength, reaction and finger dexterity were less affected, while the intelligence did not decline, but rise.
Adult ; Aerospace Medicine ; Aircraft ; Computer Simulation ; Ergonomics ; Heat Stress Disorders ; physiopathology ; Hot Temperature ; adverse effects ; Humans ; Male ; Young Adult

OBJECTIVETo study the expression and the possible role of JWA protein in oxidative stress-induced damage of MCF-7 cells, especially the relationship between JWA and heat shock proteins (HSPs).

METHODSMCF-7 cells were exposed to different concentration of H(2)O(2) (0.01,0.10, 1.00 mmol/L) for different time (10, 30, 60 and 180 min) respectively. DNA damage was detected by using DNA gel electrophoresis. The MTT assay was used to analyze the effect of H(2)O(2) on the cytotoxicity and relative cell proliferation ratio of the cells. The expressions of JWA, HSP70, HSP27 and HSF1 were determined by Western-blot.

RESULTSThe inhibitory effect on MCF-7 cells viability induced by H(2)O(2) was shown a dose-and time-dependent manner and MCF-7 cells proliferation, and was almost completely inhibited by the exposure of H(2)O(2) at 1.00 mmol/L for 180 min. Hydrogen peroxide treatment of MCF-7 cells caused oxidative stress which up-regulated the expressions of JWA, HSP70 and heat shock factor 1 (HSF1) in a dose-dependent manner, and the expression pattern of JWA was very similar to those of HSP70 and HSF1 but not to HSP27.

CONCLUSIONJWA might enhance intracellular defenses against H(2)O(2)-induced oxidative damage in human breast carcinoma cells. JWA is determined functioning as an effective environmental responsive protein and as a parallel molecule of HSP70 actively participates in the signal pathways of oxidative damage which might be regulated by HSF1.

Cell Line, Tumor ; DNA Damage ; drug effects ; DNA-Binding Proteins ; biosynthesis ; Dose-Response Relationship, Drug ; Female ; HSP27 Heat-Shock Proteins ; HSP70 Heat-Shock Proteins ; biosynthesis ; Heat Shock Transcription Factors ; Heat-Shock Proteins ; biosynthesis ; Humans ; Hydrogen Peroxide ; adverse effects ; Intracellular Signaling Peptides and Proteins ; Neoplasm Proteins ; biosynthesis ; Oxidative Stress ; drug effects ; Transcription Factors ; biosynthesis ; Up-Regulation

OBJECTIVEThe objective was to observe damage of hippocampus in rats after exposure to infrasound, and to assess HSP70 expression in hippocampus.

METHODSSD rats in the experimental group were exposed to 140 dB (8 Hz) infrasound for 2 h per day for 3 days. The morphology of the hippocampus was examined by transmission electronic microscopic (TEM). Cell apoptosis was observed by TUNEL staining at 0 h, 24 h, 48 h, and 2 w after exposure. HSP70 expression was detected by immunohistochemistry (IHC) and Western blotting (WB).

RESULTSTEM showed that hippocampus was significantly damaged by exposure, and exhibited recovery 1 week after exposure. The TUNEL data showed that neuronal apoptosis after exposure was significantly higher than in the control rats at 24 h and 48 h, and the apoptotic cells decreased one week after exposure. IHC and WB showed HSP70 expression was significantly higher in the exposed rats, peaked at 24 h.

CONCLUSIONExposure to 140 dB (8 Hz) infrasound for 2 h per day for 3 days appeared to induce damage to the hippocampus of rats, based on changes in ultrastructure and increased cell apoptosis. However, recovery from the damage occurred overtime. HSP70 expression also increased after the exposure and decreased by 48.

Animals ; Apoptosis ; Blotting, Western ; HSP70 Heat-Shock Proteins ; genetics ; metabolism ; Hippocampus ; radiation effects ; Immunohistochemistry ; In Situ Nick-End Labeling ; Male ; Rats ; Rats, Sprague-Dawley ; Sound ; adverse effects

Heat stroke is a potentially fatal disorder that's caused by an extreme elevation in body temperature. We report here an unusual case of multiple organ failure that was caused by classical, nonexertional heat stroke due to taking a warm bath at home. A 68 year old diabetic man was hospitalized for loss of consciousness. He was presumed to have been in a warm bath for 3 hrs and his body temperature was 41 degrees C. Despite cooling and supportive care, he developed acute renal failure, disseminated intravascular coagulation (DIC) and fulminant liver failure. Continuous venovenous hemofiltration was started on day 3 because of the progressive oligouria and severe metabolic acidosis. On day 15, septic ascites was developed and Acinetobacter baumanii and Enterococcus faecium were isolated on the blood cultures. In spite of the best supportive care, the hepatic failure and DIC combined with septic peritonitis progressed; the patient succumbed on day 25.
Multiple Organ Failure/*etiology ; Male ; Liver Failure/*etiology ; Kidney Failure/*etiology ; Humans ; Heat Stroke/*complications/etiology ; Fatal Outcome ; Baths/*adverse effects ; Aged