Adult ; Dimethylformamide ; analysis ; toxicity ; Dose-Response Relationship, Drug ; Humans ; Liver ; drug effects ; Male ; Middle Aged ; Occupational Exposure ; statistics & numerical data ; Physical Examination ; statistics & numerical data

China ; epidemiology ; Humans ; Occupational Diseases ; epidemiology ; prevention & control ; Surveys and Questionnaires ; Trimethyltin Compounds ; analysis ; poisoning

Chromatography, Gas ; Humans

Chlorine ; Computer Simulation ; Computers, Analog ; Diffusion ; Software

Acetamides ; metabolism ; toxicity

Noise, Occupational ; prevention & control ; Occupational Health Services ; standards ; Threshold Limit Values

Female ; Humans ; Infant, Newborn ; Maple Syrup Urine Disease ; diagnosis ; therapy

OBJECTIVETo evaluate the effects of prenatal stress on neurological functions after middle cerebral artery occlusion (MCAO) in adult offspring rats.

METHODSPregnant rats were randomly assigned to prenatal stress treatment, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment. Adult male offspring rats were subjected to transient focal cerebral ischemia by MCAO. They were randomly divided into four groups: sham group, prenatal stress + sham group, MCAO group and prenatal stress + MCAO group (n = 10). After 24 hours of reperfusion, the neurological deficits were evaluated. The infarct size, cell apoptosis and expression of Caspase 3, cleaved Caspase 3 and Bcl-2 were detected.

RESULTSCompared with MCAO group, the neurological deficits, infarct size and apoptotic cells in prenatal stress + MCAO group were increased significantly (all P < 0.05). The expressions of Caspase 3 and cleaved Caspase 3 were much greater in prenatal stress + MCAO group than those of MCAO group, while the expression of Bcl-2 was significantly decreased in prenatal stress + MCAO group compared with MCAO group (all P < 0.05).

CONCLUSIONPrenatal stress might exacerbate neuroloeical deficits in the offspring rats after MCAO by increasing cell apoptosis.

Animals ; Apoptosis ; Caspase 3 ; metabolism ; Female ; Infarction, Middle Cerebral Artery ; physiopathology ; Ischemic Attack, Transient ; physiopathology ; Male ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological

Air ; analysis ; Chromatography, Gas ; methods ; Ethylene Oxide ; analysis ; Furans ; analysis ; Methylene Chloride ; analysis ; Workplace

Biomarkers ; blood ; Dimethylformamide ; pharmacokinetics ; Humans ; Occupational Exposure