Studying the lipid peroxidation index, morphology and apoptosis in testis of male BALB/c mice exposed to polybrominated diphenyl ether (BDE-209) / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the lipid peroxidation and the testicular morphological change induced by decabrominated diphenyl ether (BDE-209) in male BALB/c mice.</p><p><b>METHODS</b>Twenty one male BALB/c mice were randomly divided into three groups: the high exposure group (500 mg/kg BDE-209), the low exposure group (200 mg/kg BDE-20) and control group (normal saline). The mice were exposed by gavage one time a day for 6 weeks, then were sacrificed. Body weight, testis weight, malonyldialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) in testis were examined. The morphological alteration of testis was observed. TUNEL assay was used to detect the apoptosis in testicular cells.</p><p><b>RESULTS</b>Body weight and testis weight in high and low exposure groups were (21.6140 +/- 2.3550) g, (20.8000 +/- 1.7630) g and (0.1859 +/- 0.0349) g, (0.1718 +/- 0.0266) g, respectively, which were significantly lower than those (27.7570 +/- 1.2880) g and (0.2302 +/- 0.0335) g in the control group (P < 0.05); the testis coefficient in high exposure group was (0.8640% +/- 0.1706%), which was significantly higher than that (0.8329 +/- 0.1386%) in the control group (P < 0.05). The GSH level and SOD activities of testis in 2 BDE-209 groups were 0.044 +/- 0.006, 0.039 +/- 0.005 nmol/mg prot, and 0.735 +/- 0.179, 0.907 +/- 0.198 U/mg prot, respectively, which were significantly lower than those (0.052 +/- 0.067) mol/mg and (1.161 +/- 0.188) U/mg in the control group (P < 0.05). The levels of MDA in 2 BDE-209 groups were (2.365 +/- 0.339) and (1.752 +/- 0.366) nmol/mg prot, which were significantly higher than that (1.173 +/- 0.232 nmol/mg prot) in control group (P < 0.05). there were significant differences of SOD and MDA levels between high exposure group and low exposure group (P < 0.05). Histological examination showed that the number of spermatogenic cells and layer were decreased significantly in 2 exposure groups as compared with control group. TUNEL assay showed that apoptosis cells appeared in 2 exposure groups.</p><p><b>CONCLUSION</b>BDE-209 changed lipid peroxidation in male BALB/c mice testis and caused toxic effects on the testis.</p>

Effects of mitogen-activated protein kinases signaling pathway proteins on kidney injury in mice exposed subchronically to cadmium / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of mitogen activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) on kidney injury in female BALB/c mice exposed to cadmium.</p><p><b>METHOD</b>Twenty-one female BALB/c mice were randomly divided into 3 groups, i.e. control group, low Cd exposure group (2.5 µmol/kg) and high Cd exposure group (10 µmol/kg) were exposed to normal saline, 2.5, 10 µmol/kg Cd, respectively, 3 times a week for 14 weeks. The kidney slice were stained by HE, PAS and Masson staining to observe the morphological changes. The expression levels of pERK, ERK, pp38, p38, pJNK and JNK proteins in kidneys were tested by Western blot assay.</p><p><b>RESULTS</b>The ratios of pERK/ERK, pp38/p38, pJNK/JNK in high Cd group were higher than those in the control group (P < 0.05). The ratio of pERK/ERK in low Cd group was higher than control group (P < 0.05). The expression levels of bcl-2, bax proteins and the ratio of bcl-2 to bax in Cd exposure groups decreased significantly, as compared with the control group (P < 0.05). The impairment of renal glomeruli and tubules were observed in HE, PAS and Masson staining slices of kidneys in mice exposed to Cd.</p><p><b>CONCLUSION</b>CdCl2 may induced renal injury by affecting the expression levels of MAPK.</p>

Effect of exposure to higher decabrominated diphenyl ether (PBDE-209) on learning and memory functions of BALB/c mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of exposure to decabrominated diphenyl ether (PBDE-209) on learning and memory of BALB/c mice.</p><p><b>METHODS</b>Eighteen female BALB/c mice were randomized divided into 3 groups and gavaged with peanut oil in the control groups and 300, 1500 mg x kg(-1)xd(-1) PBDE-209 in peanut oil daily in two exposed groups respectively for 4 weeks. The learning and memory ability of mice were tested by the Morris water maze and the shuttling box respectively. The body weight and organs index were measured and the acetylcholinesterase and butyrylcholinesterase activity in brain were determined. The liver histopathological examination was performed.</p><p><b>RESULTS</b>The heart index in high dose PBDE-209 group was higher than that of the low dose PBDE-209 group (P < 0.05). The results of Morris water maze showed that escape latency period was significantly shorter than the control group (F = 3.134, P < 0.05). The swimming time in the second quadrant of low dose PBDE-209 group was (15.78 +/- 10.92) s, significantly shorter compared with the swimming time in the second quadrant of the control group's [(28.80 +/- 8.67) s] (P < 0.05). There was no significant difference in the times of active avoidance in the shuttling between three groups (F = 3.423, P = 0.06). There were no significant differences in acetylcholinesterase and butyrylcholinesterase activity in brain of PBDE-209 groups compared with the control group (P > 0.05). Histologically liver damages in structure such as adipose degeneration and swelling were observed in PBDE groups.</p><p><b>CONCLUSION</b>Exposure to PBDE-209 slightly impairs the space learning and memory ability of BALB/c mice, and it has some hepatotoxicity.</p>

Oxidative stress of decabromodiphenylether in mice brain tissue / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the oxidative stress induced by decabromodiphenylether (PBDE-209) in the cerebral cortex, hippocampus, cerebellum and striatum of mice.</p><p><b>METHODS</b>Twenty-eight male BALB/c mice were randomized divided into four groups with seven mice in each: solvent control, blank control, low (200 mg/kg) and high (500 mg/kg) dose groups. Test substances were administered by gavage and mice were sacrificed 6 weeks after treatment. Malonyldialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) in cerebral cortex, hippocampus, cerebellum and striatum were examined.</p><p><b>RESULTS</b>The content of MDA in cerebral cortex, cerebellum, striatum and hippocampus in high dose group was (92.25 ± 36.64), (4.24 ± 1.15), (12.92 ± 4.30), (12.12 ± 6.39) nmol/mg pro respectively, higher than that in blank group [(56.713 ± 6.44), (2.42 ± 1.41), (4.05 ± 2.23), (4.91 ± 1.60) nmol/mg pro] and the difference was statistically significant (P < 0.05); T-SOD activity in cerebral cortex, cerebellum and striatum in low dose group was (182.48 ± 11.59), (6.67 ± 1.56), (35.48 ± 21.98) U/mg pro respectively, lower than that in blank group [(277.76 ± 106.70), (18.02 ± 16.40), (63.57 ± 20.83) U/mg pro] and the difference was statistically significant (P < 0.05); in high dose group the T-SOD activity in hippocampus was(59.26 ± 37.09) U/mg pro, lower than that in blank group [(93.28 ± 21.75) U/mg pro] and the difference was statistically significant (P < 0.05); The content of GSH in cerebral cortex, cerebellum and striatum in high dose group was (40.98 ± 13.19), (3.55 ± 1.55), (24.46 ± 11.30) mg/g pro respectively, lower than that in blank group [(75.79 ± 26.51), (8.01 ± 3.23), (44.52 ± 13.15) mg/g pro and the difference was statistically significant (P < 0.05); while the content of GSH in hippocampus was not decreased significantly compared with the blank group (P > 0.05).</p><p><b>CONCLUSION</b>PBDE-209 could induce oxidative stress in nervous tissue. The tissue oxidative damage might be one of the primary mechanisms of neurotoxicity of PBDE-209.</p>

Learning and Memory Damage Induced by Formaldehyde and Protective Effect of N-acetyi-cysteine in Mice / 环境与健康杂志

Objective To explore the adverse effects of formaldehyde(FA)on learning and memory ability of mice and the antagonistic effect of N-acetyl-cysteine(NAC),an antioxidant.Methods Thirty-four ICR mice were randomly divided into four groups,the control(NS,n=8),treated with FA(15 mg/kg,n=9),treated with NAC(100 mg/kg,n=8),treated with FA(15 mg/kg) plus NAC(100 mg/kg,n=9),the treatment was conducted by intraperitoneal injection once a day for seven consecutive days.On the eighth day,the learning and memory ability were tested by using water labyrinth task for seven consecutive days.Results The mice in FA group behaved excited,restless and then turned to repose,moveless and clustering,but this phenomena was not seen in the other groups.There was no significant difference in the body weight of mice among groups.As for learning,latent period in the FA group [(27.15?2.66)s] was significantly longer than that in the control group [(15.83?2.82)s] and the FA+ NAC group[(14.98?2.66)s],and revealed statistical significance(P

Studies on fluoride concentration and cholinesterase activity in rat hippocampus / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the accumulation of fluoride in rat hippocampus and its effect on cholinesterase activity.</p><p><b>METHODS</b>Rats were subchronically exposed to NaF, and fluoride concentration and cholinesterase activity in rat hippocampus were determined.</p><p><b>RESULTS</b>Fluoride concentration in rat hippocampus was significantly correlated with the dosage of fluoride, and there were significant differences among high dosage group [(13.03 +/- 1.79) micro g/g], low dosage group [(9.83 +/- 0.92) micro g/g] and control [(8.27 +/- 1.11) micro g/g], P < 0.01. Acetylcholinesterase activities among three groups [(0.111 +/- 0.031) micro mol/mg, (0.143 +/- 0.025) micro mol/mg, (0.183 +/- 0.027) micro mol/mg] were also significantly different (P < 0.01), which was negatively correlated with fluoride concentration in rat hippocampus (r = -0.700, P < 0.01). The activity of butylcholinesterase in high dosage group [(0.041 +/- 0.010) micro mol/mg] was different from that of control [(0.067 +/- 0.025) micro mol/mg, P < 0.05], but the activity was not significantly related with fluoride concentration in rat hippocampus (r = -0.317, P = 0.094).</p><p><b>CONCLUSION</b>Fluoride may go through the blood-brain barrier and accumulate in rat hippocampus, and inhibit the activity of cholinesterase.</p>