中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2013年
9期
799-805
,共7页
姚茂琳%张爱华%于春%徐玉艳%胡勇%肖婷婷%王蕾
姚茂琳%張愛華%于春%徐玉豔%鬍勇%肖婷婷%王蕾
요무림%장애화%우춘%서옥염%호용%초정정%왕뢰
砷中毒%煤%大鼠%毒性
砷中毒%煤%大鼠%毒性
신중독%매%대서%독성
Arsenic poisoning%Coal%Rat%Toxicity
目的 采用高砷煤烘烤的玉米粉为主要原料配制饲料喂饲大鼠,建立燃煤型砷中毒大鼠模型.方法 采用健康断乳Wistar大鼠50只,按体重用随机数字法分为5组(正常对照组,饮水型砷中毒组,低砷、中砷和高砷粮食污染组),每组10只.正常组和饮水型砷中毒组喂饲不含砷的标准饲料,饮水型砷中毒大鼠饮用100 mg/L的As2O3水溶液,各粮食砷污染组分别喂饲含砷25、50、100 mg/kg的饲料,染毒时间3个月.观察大鼠一般情况,检测其尿砷、毛发砷、肝砷和肾砷含量;观察肝、肾常规病理学改变及肝脏超微结构改变;测定检测肝肾功能指标.结果 饮水型砷中毒组、低砷、中砷和高砷粮食污染组尿砷[中位数(最大值~最小值)分别为3055.59 (722.43~ 6389.05)、635.96(367.85 ~1551.31)、1453.84(593.27~5302.94)、3101.11 (666.64~6858.61) μg/g肌酐]、毛发砷[分别为(23.07±10.38)、(8.87±3.31)、(12.43±6.65)和(25.68±7.16)μg/g]、肝脏中砷[分别为(5.68±3.13)、(2.64±1.52)、(3.89±1.76)和(5.34±2.78)μg/g]、肾脏中砷[分别为(6.90±1.94)、(3.48±1.96)、(5.03±2.08)和(7.02±1.62) μg/g]含量均高于正常对照组[分别为86.70(49.71~ 106.104) μg/g肌酐、(1.28±0.37) μg/g、(1.01 ±0.34)μg/g和(1.82±1.09) μg/g],差异有统计学意义(P<0.05).电镜下可见染砷组大鼠肝细胞质线粒体减少、嵴模糊、部分嵴消失,粗面内质网减少,核形态不规则、凹凸不平.中、高砷粮食污染组天冬氨酸氨基转移酶(AST)[(196.17±46.18)、(212.40±35.14) U/L]和总胆汁酸(TBA)[(11.74±4.07)、(19.19±4.68) μmol/L],均高于对照组[分别为(143.10±29.13) U/L、(6.23±2.95)μmol/L];高砷粮食污染组谷胱甘肽硫转移酶(GST)、γ-谷氨酰转肽酶(GGT)和尿素氮(BUN)[分别为(196.21±47.38)U/L、(1.71±0.66) U/L、(9.54±1.95) mmol/L]高于正常对照组[分别为(134.93±24.80)U/L、(0.75±0.36) U/L、(7.67±1.02) mmol/L];低、中、高砷粮食污染组胆碱酯酶(CHE)[分别为(259.90±52.71) U/L、(263.44±66.06) U/L、(244.90±36.14) U/L],高砷粮食污染组总蛋白(TP) [(62.64±5.50) g/L]均低于正常对照组[分别为(448.33±59.67) U/L、(69.38 ±4.24) g/L];高砷粮食污染组TBA[(19.19±4.68) μmol/L]高于饮水型砷中毒组[(15.15±2.64) μmol/L],差异均有统计学意义(P<0.05).结论 成功建立燃煤污染型砷中毒大鼠模型.
目的 採用高砷煤烘烤的玉米粉為主要原料配製飼料餵飼大鼠,建立燃煤型砷中毒大鼠模型.方法 採用健康斷乳Wistar大鼠50隻,按體重用隨機數字法分為5組(正常對照組,飲水型砷中毒組,低砷、中砷和高砷糧食汙染組),每組10隻.正常組和飲水型砷中毒組餵飼不含砷的標準飼料,飲水型砷中毒大鼠飲用100 mg/L的As2O3水溶液,各糧食砷汙染組分彆餵飼含砷25、50、100 mg/kg的飼料,染毒時間3箇月.觀察大鼠一般情況,檢測其尿砷、毛髮砷、肝砷和腎砷含量;觀察肝、腎常規病理學改變及肝髒超微結構改變;測定檢測肝腎功能指標.結果 飲水型砷中毒組、低砷、中砷和高砷糧食汙染組尿砷[中位數(最大值~最小值)分彆為3055.59 (722.43~ 6389.05)、635.96(367.85 ~1551.31)、1453.84(593.27~5302.94)、3101.11 (666.64~6858.61) μg/g肌酐]、毛髮砷[分彆為(23.07±10.38)、(8.87±3.31)、(12.43±6.65)和(25.68±7.16)μg/g]、肝髒中砷[分彆為(5.68±3.13)、(2.64±1.52)、(3.89±1.76)和(5.34±2.78)μg/g]、腎髒中砷[分彆為(6.90±1.94)、(3.48±1.96)、(5.03±2.08)和(7.02±1.62) μg/g]含量均高于正常對照組[分彆為86.70(49.71~ 106.104) μg/g肌酐、(1.28±0.37) μg/g、(1.01 ±0.34)μg/g和(1.82±1.09) μg/g],差異有統計學意義(P<0.05).電鏡下可見染砷組大鼠肝細胞質線粒體減少、嵴模糊、部分嵴消失,粗麵內質網減少,覈形態不規則、凹凸不平.中、高砷糧食汙染組天鼕氨痠氨基轉移酶(AST)[(196.17±46.18)、(212.40±35.14) U/L]和總膽汁痠(TBA)[(11.74±4.07)、(19.19±4.68) μmol/L],均高于對照組[分彆為(143.10±29.13) U/L、(6.23±2.95)μmol/L];高砷糧食汙染組穀胱甘肽硫轉移酶(GST)、γ-穀氨酰轉肽酶(GGT)和尿素氮(BUN)[分彆為(196.21±47.38)U/L、(1.71±0.66) U/L、(9.54±1.95) mmol/L]高于正常對照組[分彆為(134.93±24.80)U/L、(0.75±0.36) U/L、(7.67±1.02) mmol/L];低、中、高砷糧食汙染組膽堿酯酶(CHE)[分彆為(259.90±52.71) U/L、(263.44±66.06) U/L、(244.90±36.14) U/L],高砷糧食汙染組總蛋白(TP) [(62.64±5.50) g/L]均低于正常對照組[分彆為(448.33±59.67) U/L、(69.38 ±4.24) g/L];高砷糧食汙染組TBA[(19.19±4.68) μmol/L]高于飲水型砷中毒組[(15.15±2.64) μmol/L],差異均有統計學意義(P<0.05).結論 成功建立燃煤汙染型砷中毒大鼠模型.
목적 채용고신매홍고적옥미분위주요원료배제사료위사대서,건립연매형신중독대서모형.방법 채용건강단유Wistar대서50지,안체중용수궤수자법분위5조(정상대조조,음수형신중독조,저신、중신화고신양식오염조),매조10지.정상조화음수형신중독조위사불함신적표준사료,음수형신중독대서음용100 mg/L적As2O3수용액,각양식신오염조분별위사함신25、50、100 mg/kg적사료,염독시간3개월.관찰대서일반정황,검측기뇨신、모발신、간신화신신함량;관찰간、신상규병이학개변급간장초미결구개변;측정검측간신공능지표.결과 음수형신중독조、저신、중신화고신양식오염조뇨신[중위수(최대치~최소치)분별위3055.59 (722.43~ 6389.05)、635.96(367.85 ~1551.31)、1453.84(593.27~5302.94)、3101.11 (666.64~6858.61) μg/g기항]、모발신[분별위(23.07±10.38)、(8.87±3.31)、(12.43±6.65)화(25.68±7.16)μg/g]、간장중신[분별위(5.68±3.13)、(2.64±1.52)、(3.89±1.76)화(5.34±2.78)μg/g]、신장중신[분별위(6.90±1.94)、(3.48±1.96)、(5.03±2.08)화(7.02±1.62) μg/g]함량균고우정상대조조[분별위86.70(49.71~ 106.104) μg/g기항、(1.28±0.37) μg/g、(1.01 ±0.34)μg/g화(1.82±1.09) μg/g],차이유통계학의의(P<0.05).전경하가견염신조대서간세포질선립체감소、척모호、부분척소실,조면내질망감소,핵형태불규칙、요철불평.중、고신양식오염조천동안산안기전이매(AST)[(196.17±46.18)、(212.40±35.14) U/L]화총담즙산(TBA)[(11.74±4.07)、(19.19±4.68) μmol/L],균고우대조조[분별위(143.10±29.13) U/L、(6.23±2.95)μmol/L];고신양식오염조곡광감태류전이매(GST)、γ-곡안선전태매(GGT)화뇨소담(BUN)[분별위(196.21±47.38)U/L、(1.71±0.66) U/L、(9.54±1.95) mmol/L]고우정상대조조[분별위(134.93±24.80)U/L、(0.75±0.36) U/L、(7.67±1.02) mmol/L];저、중、고신양식오염조담감지매(CHE)[분별위(259.90±52.71) U/L、(263.44±66.06) U/L、(244.90±36.14) U/L],고신양식오염조총단백(TP) [(62.64±5.50) g/L]균저우정상대조조[분별위(448.33±59.67) U/L、(69.38 ±4.24) g/L];고신양식오염조TBA[(19.19±4.68) μmol/L]고우음수형신중독조[(15.15±2.64) μmol/L],차이균유통계학의의(P<0.05).결론 성공건립연매오염형신중독대서모형.
Objective To establish coal arsenic poisoning rat model by feeding the rats with the corn powder baked by high arsenic coal as the main raw material.Methods Fifty Wistar rats,healthy,were randomly divided into 5 groups according to the figures of their weights,including control group,drinking arsenic poisoning water group,low,medium and high arsenic contaminated grain group,10 rats for each.Rats in control group and drinking arsenic poisoning water group were fed with standard feed without any arsenic containing.Rats in water group would drink 100 mg/L As2O3 solution and the rats in arsenic grain groups would be fed with the arsenic contaminated grain at the dose of 25,50 and 100 mg/kg,respectively.The duration would last for 3 months.General situation and weight were observed.At the same time,the arsenic contents of urine,hair,liver and kidney of the rats in each group were detected,as well as the histopathology changes of liver and kidney,and the ultra structure of liver was observed.Results The arsenic contents of urine (median (min-max)) of the rats in the arsenic water group,low,medium and high arsenic grain groups were separately 3055.59 (722.43-6389.05),635.96 (367.85-1551.31),1453.84 (593.27-5302.94) and 3101.11(666.64-6858.61) μg Cr; while the arsenic contents of hair of the rats in the above groups were separately (23.07 ± 10.38),(8.87 ± 3.31),(12.43 ±6.65) and (25.68 ± 7.16) μg/g; the arsenic contents of liver of the rats in the above groups were separately (5.68 ± 3.13),(2.64 ± 1.52),(3.89 ± 1.76) and (5.34 ± 2.78) μg/g; and the arsenic contents of kidney were separately (6.90 ± 1.94),(3.48 ± 1.96),(5.03 ± 2.08) and (7.02 ± 1.62) μg/g; which were all significantly higher than those in the control group (86.70 (49.71-106.104) μg/g Cr,(1.28 ± 0.37) μg/g,(1.01 ± 0.34) μg/g and (1.82 ± 1.09) μg/g,respectively).The difference showed significance (P < 0.05).Under electron microscope detection,we observed the reduction of mitochondrial,the blurred mitochondrial cristae,some disappeared ridges,the reduced rough endoplasmic reticulum,and irregular uneven nuclear in the liver cells of rats in arsenic contaminated grain group.The contents of aspartate transaminase (AST) and total bile acid (TBA) in medium and high arsenic contaminated grain group were respectively (196.17 ± 46.18),(212.40 ± 35.14) U/L and (11.74 ± 4.07),(19.19 ± 4.68) μmol/L,which were higher than it in the control group (separately (143.10 ± 29.13) U/L and (6.23 ± 2.95) μmol/L).The contents of glutathione-S-transferases (GST),γ-glutamyltranspeptidase (GGT) and blood urea nitrogen (BUN)in high arsenic contaminated grain group were separately (196.21 ± 47.38) U/L,(1.71 ± 0.66) U/L,(9.54 ± 1.95) mmol/L,which were higher than that in the control group ((134.93 ± 24.80) U/L,(0.75 ± 0.36) U/L,(7.67 ± 1.02) mmol/L,respectively).The contents of cholinesterase (CHE) in low,medium and high arsenic contaminated grain group were separately (259.90 ± 52.71) U/L,(263.44 ± 66.06) U/L and (244.90 ± 36.14) U/L,the contents of total protein(TP) in rats of high arsenic contaminated grain group were (62.64 ± 5.50)g/L,which was all lower than that in the control group ((448.33 ± 59.67) U/L,(69.38 ± 4.24) g/L,respectively).The contents of TBA in high arsenic contaminated grain group ((19.19 ± 4.68) μmol/L) was higher than that in drinking water arsenic poisoning group ((15.15 ±2.64)μmoL/L).The differences of the above indexes were all significant (P < 0.05).Conclusion The results showed the arsenic poisoning rat model produced by coal-burning were successfully established.