中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2010年
12期
900-903
,共4页
张照祥%王兴华%邹立巍%丁书姝%翟金霞
張照祥%王興華%鄒立巍%丁書姝%翟金霞
장조상%왕흥화%추립외%정서주%적금하
多溴联苯类%氧化性应激%脂质过氧化作用
多溴聯苯類%氧化性應激%脂質過氧化作用
다추련분류%양화성응격%지질과양화작용
Polybrominated biphenyls%Oxidative stress%Lipid peroxidation
目的 研究十溴联苯醚(decabromodiphenylether,PBDE-209)对小鼠大脑皮层、海马、纹状体和小脑组织诱导的氧化应激作用.方法 28只雄性BALB/c小鼠,随机分为4组,即溶剂对照组、空白对照组、低剂量染毒组(200mg/kg)和高剂量染毒组(500mg/kg),每组7只,小鼠经口灌胃染毒6周后断头处死,测定小鼠大脑皮层、海马、小脑和纹状体中丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)活力以及谷胱甘肽(GSH)含量.结果 高剂量染毒组小鼠大脑皮层、小脑、纹状体和海马组织中MDA含量分别为(92.25±36.64)、(4.24±1.15)、(12.92±4.30)、(12.12±6.39)nmol/mgpro,高于空白对照组[分别为(56.71±36.44)、(2.42±1.41)、(4.05±2.23)、(4.91±1.60)nmol/mg pro],差异均有统计学意义(P＜0.05);低剂量染毒组小鼠大脑皮层、小脑和纹状体中T-SOD活力分别为(182.48±11.59)、(6.67±1.56)、(35.48±21.98)U/mg pro,低于空白对照组[分别为(277.76±106.70)、(18.02±16.40)、(63.57±20.83)U/mg pro],差异均有统计学意义(P＜0.05);高剂量染毒组小鼠海马组织中T-SOD活力为(59.26±37.09)U/mg pro,低于空白对照组[(93.28±21.75)U/mg pro],差异有统计学意义(P＜0.05);高剂量染毒组小鼠大脑皮层、小脑、纹状体中GSH含量分别为(40.98±13.19)、(3.55±1.55)、(24.46±11.30)mg/g pro,低于空白对照组[分别为(75.79±26.51)、(8.01±3.23)、(44.52±13.15)mg/g pro],差异均有统计学意义(P＜0.05);而染毒小鼠海马组织中GSH含量与溶剂对照组的差异无统计学意义(P＞0.05).结论 PBDE-209可以引起神经组织的脂质过氧化反应增强.PBDE-209导致神经组织的氧化损伤可能在动物神经毒性中起重要作用.
目的 研究十溴聯苯醚(decabromodiphenylether,PBDE-209)對小鼠大腦皮層、海馬、紋狀體和小腦組織誘導的氧化應激作用.方法 28隻雄性BALB/c小鼠,隨機分為4組,即溶劑對照組、空白對照組、低劑量染毒組(200mg/kg)和高劑量染毒組(500mg/kg),每組7隻,小鼠經口灌胃染毒6週後斷頭處死,測定小鼠大腦皮層、海馬、小腦和紋狀體中丙二醛(MDA)含量、總超氧化物歧化酶(T-SOD)活力以及穀胱甘肽(GSH)含量.結果 高劑量染毒組小鼠大腦皮層、小腦、紋狀體和海馬組織中MDA含量分彆為(92.25±36.64)、(4.24±1.15)、(12.92±4.30)、(12.12±6.39)nmol/mgpro,高于空白對照組[分彆為(56.71±36.44)、(2.42±1.41)、(4.05±2.23)、(4.91±1.60)nmol/mg pro],差異均有統計學意義(P＜0.05);低劑量染毒組小鼠大腦皮層、小腦和紋狀體中T-SOD活力分彆為(182.48±11.59)、(6.67±1.56)、(35.48±21.98)U/mg pro,低于空白對照組[分彆為(277.76±106.70)、(18.02±16.40)、(63.57±20.83)U/mg pro],差異均有統計學意義(P＜0.05);高劑量染毒組小鼠海馬組織中T-SOD活力為(59.26±37.09)U/mg pro,低于空白對照組[(93.28±21.75)U/mg pro],差異有統計學意義(P＜0.05);高劑量染毒組小鼠大腦皮層、小腦、紋狀體中GSH含量分彆為(40.98±13.19)、(3.55±1.55)、(24.46±11.30)mg/g pro,低于空白對照組[分彆為(75.79±26.51)、(8.01±3.23)、(44.52±13.15)mg/g pro],差異均有統計學意義(P＜0.05);而染毒小鼠海馬組織中GSH含量與溶劑對照組的差異無統計學意義(P＞0.05).結論 PBDE-209可以引起神經組織的脂質過氧化反應增彊.PBDE-209導緻神經組織的氧化損傷可能在動物神經毒性中起重要作用.
목적 연구십추련분미(decabromodiphenylether,PBDE-209)대소서대뇌피층、해마、문상체화소뇌조직유도적양화응격작용.방법 28지웅성BALB/c소서,수궤분위4조,즉용제대조조、공백대조조、저제량염독조(200mg/kg)화고제량염독조(500mg/kg),매조7지,소서경구관위염독6주후단두처사,측정소서대뇌피층、해마、소뇌화문상체중병이철(MDA)함량、총초양화물기화매(T-SOD)활력이급곡광감태(GSH)함량.결과 고제량염독조소서대뇌피층、소뇌、문상체화해마조직중MDA함량분별위(92.25±36.64)、(4.24±1.15)、(12.92±4.30)、(12.12±6.39)nmol/mgpro,고우공백대조조[분별위(56.71±36.44)、(2.42±1.41)、(4.05±2.23)、(4.91±1.60)nmol/mg pro],차이균유통계학의의(P＜0.05);저제량염독조소서대뇌피층、소뇌화문상체중T-SOD활력분별위(182.48±11.59)、(6.67±1.56)、(35.48±21.98)U/mg pro,저우공백대조조[분별위(277.76±106.70)、(18.02±16.40)、(63.57±20.83)U/mg pro],차이균유통계학의의(P＜0.05);고제량염독조소서해마조직중T-SOD활력위(59.26±37.09)U/mg pro,저우공백대조조[(93.28±21.75)U/mg pro],차이유통계학의의(P＜0.05);고제량염독조소서대뇌피층、소뇌、문상체중GSH함량분별위(40.98±13.19)、(3.55±1.55)、(24.46±11.30)mg/g pro,저우공백대조조[분별위(75.79±26.51)、(8.01±3.23)、(44.52±13.15)mg/g pro],차이균유통계학의의(P＜0.05);이염독소서해마조직중GSH함량여용제대조조적차이무통계학의의(P＞0.05).결론 PBDE-209가이인기신경조직적지질과양화반응증강.PBDE-209도치신경조직적양화손상가능재동물신경독성중기중요작용.
Objective To study the oxidative stress induced by decabromodiphenylether(PBDE-209)in the cerebral cortex,hippocampus,cerebellum and striatum of mice.Methods Twenty-eight male BALB/c mice were randomizedly 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.Results 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).Conclusion 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.
