Comparative studies on the effects of semipurified and commercial diet on longevity and spontaneous and induced lesions in the Syrian golden hamster

Syrian golden hamsters were fed a semipurified or commercial diet from weaning throughout life. Bis(2‐oxopropyl)nitrosamine (BOP) was administered at 8 weeks of age (10 mg/kg body wt, sc). Longevity was improved by 26% and 36% increases in the mean life‐spans of male and female hamsters, respectively, fed the semipurified diets. Carcinogen treatment did not alter survival. The age‐adjusted occurrence rates of pancreatic ductular proliferation, carcinomas, adenomas, and common duct polyps were higher in hamsters fed commercial diet; this indicates an earlier onset of these BOP‐induced lesions in hamsters fed this diet. However, their overall incidences were generally similar when the two diet groups were compared. Acinar cell nodules were observed only in hamsters fed semipurified diets and were elevated in BOP‐treated females. The onset of pancreatic ductular proliferation and adenomas, bile duct proliferation, parathyroid hyperplasia, and common duct papillary hyperplasia was earlier in females than in male hamsters, especially in groups fed commercial ration. Generalized vascular calcification was observed at an elevated rate and reached a higher overall incidence in hamsters fed commercial ration. The age‐adjusted rate of amyloidosis was high in female hamsters and elevated in groups that consumed the commercial ration. In addition, colitis and islet cell hyperplasia occurred more often and earlier in hamsters fed commercial ration, but gallbladder stones occurred most in animals fed semipurified diet. This paper discusses the possible association between these and other observed lesions and survival.     

褪黑素对低硒饮食大鼠脂质过氧化的影响

目的 :研究褪黑素对低硒粮喂养的大鼠脂质过氧化增强的影响 ,并讨论其可能机制。方法 :将SD大鼠分为 3组 ,分别用低硒饲料、低硒饲料加硒、低硒饲料加褪黑素灌胃饲养 ,12周时检测血Se、血GSH—Px及心肌组织、肝组织匀浆MDA水平。结果 :12周时低硒组大鼠血Se、GSH—Px较加硒组 (对照组 )显著降低 ,心肌组织、肝组织匀浆MDA均明显高于其它两组。加硒组与褪黑素组MDA无显著差异。结论 :褪黑素可以显著抑制低硒饮食大鼠脂质过氧化的增强 ,作用与其抗氧化机制有关     

Enhancement of BOP-induced pancreatic carcinogenesis in selenium-fed Syrian golden hamsters under specific dietary conditions

We measured the effects of dietary selenium (Se) on pancreatic cancer induced in Syrian golden hamsters by N-nitrosobis(2-oxopropyl)amine (BOP). The animals were fed six experimental diets that contained different combinations of the following: 0.1, 2.5, or 5.0 ppm Se from sodium selenite or 2.5 ppm Se from D,L-selenomethionine in either a low (6.0%)- or high (24.4%)-fat diet. Se treatment was begun four weeks before BOP treatment, and the high-fat diet was fed from one week after the last BOP treatment. No evidence for inhibition of pancreatic cancer by Se was observed; in fact, with some experimental conditions, high-Se diets increased the pancreatic carcinoma yield. However, the dietary conditions needed for enhancement differed between the sexes. The male hamsters that received the high-fat diet containing 2.5 ppm Se had more carcinomas than did males given the 0.1 ppm Se level. Carcinoma yields in females did not differ between these diets. Females that received 2.5 ppm Se from D,L-selenomethionine had a greater pancreatic carcinoma yield that did those given 0.1 ppm Se diet. However, carcinoma yields did not differ in males fed these diets. Acinar cell nodule yields were generally reduced in hamsters given the high-Se diets, especially when Se levels in the high-fat diets were compared. Prefeeding 0.1 or 2.5 ppm Se did not influence the elution constants of pancreatic DNA from ductal cells, indicating no effect of Se on the repair of BOP-induced, single-strand breaks in DNA from these cells. Measurements in acinar cells suggested a more rapid repair of single-strand breaks in hamsters prefed 2.5 ppm Se than in those prefed 0.1 ppm Se.     

低硒与心肌细胞氧化损伤机制及凋亡相关基因的表达

目的观察低硒对大鼠心肌组织脂质过氧化物、心肌细胞超微结构及细胞凋亡相关基因的影响。方法建立对照组、低硒组、补硒组3个组别大鼠模型,结合光镜及电镜下心肌组织及其超微结构病理变化,对其血清硒、谷胱甘肽过氧化物酶（GPx）、心肌组织匀浆丙二醛（MDA）水平及心肌细胞凋亡相关基因Bcl-2、Bax、P53蛋白表达进行检测及对比分析。结果低硒组大鼠血清硒水平及血清GPx活性水平均显著低于正常对照组和低硒加硒组,低硒组大鼠心肌组织匀浆MDA水平显著高于正常对照组和低硒加硒组。低硒组大鼠心肌线粒体膜及细胞核膜上清晰可见高电子密度反应产物聚集。低硒组大鼠心肌Bcl-2、Bax、P53的基因表达（PI％）均显著高于正常对照组大鼠;低硒组大鼠Bcl-2基因表达（PI％）显著低于低硒加硒组大鼠;而Bax、P53的基因表达（PI％）均显著高于低硒加硒组。结论低硒可以引起线粒体膜、细胞核膜磷脂过氧化损伤,进而造成心肌细胞线粒体损伤,同时可引起大鼠心肌细胞抑制凋亡基因Bcl-2和促进凋亡基因Bax、P53的基因表达相应增强,但BcF2／Bax比值相对下降,促进凋亡的发生。补硒可以诱导抑制凋亡基因Bcl-2基因表达的上调,使其基因表达增强,同时相对抑制促凋亡基因Bax和P53的表达。     

Comparative studies on the effects of semipurified and commercial diet on longevity and spontaneous and induced lesions in the Syrian golden hamster

Syrian golden hamsters were fed a semipurified or commercial diet from weaning throughout life. Bis(2-oxopropyl)nitrosamine (BOP) was administered at 8 weeks of age (10 mg/kg body wt, sc). Longevity was improved by 26% and 36% increases in the mean life-spans of male and female hamsters, respectively, fed the semipurified diets. Carcinogen treatment did not alter survival. The age-adjusted occurrence rates of pancreatic ductular proliferation, carcinomas, adenomas, and common duct polyps were higher in hamsters fed commercial diet; this indicates an earlier onset of these BOP-induced lesions in hamsters fed this diet. However, their overall incidences were generally similar when the two diet groups were compared. Acinar cell nodules were observed only in hamsters fed semipurified diets and were elevated in BOP-treated females. The onset of pancreatic ductular proliferation and adenomas, bile duct proliferation, parathyroid hyperplasia, and common duct papillary hyperplasia was earlier in females than in male hamsters, especially in groups fed commercial ration. Generalized vascular calcification was observed at an elevated rate and reached a higher overall incidence in hamsters fed commercial ration. The age-adjusted rate of amyloidosis was high in female hamsters and elevated in groups that consumed the commercial ration. In addition, colitis and islet cell hyperplasia occurred more often and earlier in hamsters fed commercial ration, but gallbladder stones occurred most in animals fed semipurified diet. This paper discusses the possible association between these and other observed lesions and survival.     

不同膳食硒水平对甲基苄基亚硝胺(NMBzA)诱发大鼠食道肿瘤及小鼠前胃肿瘤的影响

本实验对膳食中不同硒含量与NMBzA诱发大鼠食道肿瘤及小鼠前胃肿瘤的关系进行了研究。分别将断乳Wistar大鼠和断乳昆明种小鼠随机分成缺硒(硒含量<0.02ppm)组;正常硒(0.2ppm)组;补硒(2.0ppm)组;和对照组(0.2ppm)。除对照组外,各组动物灌胃给予NMBzA。其中大鼠自第5周至第18周实验结束,每周一次给药3mg/kg体重,小鼠第2～7周,每周一次给药1mg/kg体重,第8～12周,每周二次,每次0.7mg/kg体重。实验结束时分别进行病理学检查。结果大鼠食道肿瘤及小鼠前胃肿瘤发生率在各实验组间无显著性差异。     

Effect of selenium and molybdenum on methylbenzylnitrosamine-induced esophageal lesions and tissue trace metals in the rat

Thirty-six weanling male Sprague-Dawley rats were randomly assigned to one of four treatment groups: SE rats received 4.0 ppm selenium as sodium selenite in drinking water containing 1% sucrose; 15MO rats received 15 ppm molybdenum as sodium molybdate in the drinking water; 45MO rats received 45 ppm molybdenum in their water; and CON rats received distilled-deionized water containing only 1% sucrose. The esophageal carcinogen methylbenzylnitrosamine (MBN) was administered intragastrically in 10% ethanol twice per week for 5 wk at a dose of 2.5 mg/kg. MBN dosing was followed by a 12-wk period for tumor promotion. After this, heart, lungs, liver, spleen, kidneys, testes, tibia, muscle, brain and esophagus were excised. The esophagus was examined for MBN-induced lesions using dissecting and light microscopes and a portion was analyzed for Se. All other tissues were analyzed for Cu, Zn, Fe and Mn; some were also analyzed for Se and Mo. Most rats had precancerous lesions, and all rats had papillomas. There were no significant differences among the four treatment groups in the incidence and number per rat of precancerous lesions or gross papillomas. The SE group had significantly fewer carcinomas per rat than the other groups. The SE rats exhibited a number of significant differences in tissue trace element concentrations; in particular, they had higher Fe concentrations in heart, kidney and spleen than the other rats. The SE rats also had significantly greater urinary excretion of Mn and Fe, and excretion of the latter elements was significantly correlated with that of selenium.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of dietary selenium and vitamin A on biochemical parameters and survival of young among white-tailed deer (Odocoileus virginianus)

Thirty-two adult female white-tailed deer were assigned to four complete pelleted diets (+/- 45 ppm vitamin E; +/- 0.2 ppm selenium). Selenium and vitamin E concentration in the unsupplemented diet was 0.04 and 5.5 ppm, respectively. Biochemical parameters of the erythrocyte (RBC) glutathione peroxidase system and survival of off-spring to weaning were followed for 2 years. At the end of the second year, 12 male young (3 per treatment) and the remaining adults were killed, and liver and muscle parameters of the glutathione system determined. Plasma selenium (Se) and vitamin E (E) were significantly lower among unsupplemented adults within 6 months of treatment and remained essentially constant from 10 months on. In vitro hemolysis and mortality of young were affected by dietary E but not by Se. Tissue glutathione peroxidase (GSH-Px) was correlated with tissue Se in all tissues measured (RBC, liver and muscle). Tissue Se, in turn, was related to dietary Se. Thus, dietary Se deficiency (Se = 0.04 ppm) resulted in biochemical deficiency (depressed GSH-Px). This was not reflected in gross lesions among the adults, nor in increased mortality among young.     

Carcinogenic effect of arsenate in C57BL/6J/Han mice and its modulation by different dietary selenium status

In this study, carcinogenic effects of arsenate in female C57BL/6J/Han mice exposed in drinking water to 50, 200 or 500 μg As/L for 24 months were investigated. All animals were fed low-selenium diet, however half of them were supplemented with sodium selenite in drinking water (200 μg Se/L) to ensure the normal dietary level of selenium. Glutathione peroxidase activity in erythrocytes and plasma as well as selenium concentration in plasma after 3, 6, 12 and 18 months in satellite groups showed considerable decrease in animals from non-selenium supplemented groups in comparison to supplemented groups. A clear arsenic concentration-dependent increase in the number of malignant lymphoma associated with increase in the risk of death was observed (hazard ratio=0.91, 1.46, and 2.24, for 50, 200 and 500 μg As/L, respectively). No significant influence of selenium dietary status on arsenic carcinogenicity was shown. A significant association between selenium supplementation status and increased risk of death of the animals from causes other than malignant tumors was found (HR=1.79, p=0.04).     

Selenium status of term infants fed selenium-supplemented formula in a randomized dose-response trial

BACKGROUND: The optimal form and dose of selenium supplementation required to achieve indicators of selenium status equivalent to those in breastfed infants are unclear. OBJECTIVE: The objective was to evaluate the effect of fortifying infant formula (6 microg Se/L) with 2 concentrations of selenate (7 and 15 microg/L) on biochemical indicators of selenium status and growth at 16 wk in term infants. DESIGN: A randomized dose-response trial was conducted in 3 groups of term infants fed formula with different selenium concentrations [6 microg/L, F+0 (control); 13 microg/L, F+7; and 21 microg/L, F+15] and in a parallel breastfed reference group (BF; 11 +/- 2 microg Se/L). RESULTS: One hundred sixty-one (47% males) infants completed the 16-wk study. Baseline plasma selenium was 0.3 +/- 0.1 micromol/L. At 16 wk, plasma selenium had increased in all groups (P < 0.001) and was greater (P < 0.01) in the F+7 and F+15 groups and lower (P < 0.05) in the F+0 group than in the BF group. Plasma glutathione peroxidase increased in the F+15 group, decreased in the F+0 group, and, at 16 wk, was lower in the F+0 group than in the other groups (all P < 0.05). Erythrocyte selenium and glutathione peroxidase decreased in all groups (P < 0.05), but the magnitude of the change was greater in the F+0 than in the F+15 group (P < 0.05). There was no effect of selenium supplementation on growth. CONCLUSIONS: Selenate fortification of formula resulted in an increase in plasma indicators of selenium status relative to indicators observed in infants fed low-selenium-containing formula. Although the erythrocyte indicators decreased in all groups, the 21-microg/L dose (F+15 group) resulted in a smaller decrease and in higher erythrocyte selenium than did the standard formula. Supplementation of low-selenium formula to provide a net selenium concentration close to that found in the breast milk of US women (18 microg/L) may be justified.     

克山病病区粮对大鼠全血谷胱甘肽过氧化物酶活力及体内抗氧化能力的影响

1.比较了病区和非病区玉米、大米饲料及动物房常备饲料喂养的大鼠全血GSH-Px活力。结果表明:常备组高于非病区组,后者又高于病区组。同时测定的体外用维生素C氧化血红蛋白生成的高铁血红蛋白、胆绿蛋白和Heinz小体的百分率。各组雌鼠之间无显著差异,而雄鼠的结果与GSH-Px活力呈反相关。 2.喂以病区玉米饲料三个月造成乏硒的大鼠补充硒(Na_2SeO_3)50天后,血硒和红细胞GSH—Px活力均升到接近常备饲料组大鼠的水平。     

过量碘对甲状腺激素代谢的损伤及硒的干预作用

目的研究过量碘性甲状腺激素代谢紊乱的机制并寻求合适的硒干预剂量。方法140只Balb/c小鼠分为7组:正常组、过量碘组(饮水含碘3000μg/L)和5个补硒组(饮水含碘3000μg/L,硒分别为0.1、0.2、0.3、0.4和0.5mg/L),共喂养16周。放射免疫法测定血清甲状腺激素水平,砷铈催化分光光度法测定尿碘和甲状腺碘水平,测定甲状腺谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和甲状腺过氧化物酶(TPO)活性以及丙二醛(MDA)水平。结果0.1～0.5mg/L补硒组甲状腺激素水平与正常组比较差异无显著性,0.2mg/L补硒组甲状腺内碘含量较过量碘组显著下降(P<0.05),0.2～0.3mg/L补硒组甲状腺GSH-Px、SOD活性和MDA水平与正常组比较差异无显著性,0.1～0.3mg/L补硒组TPO活性与正常组比较差异无显著性。结论补充硒对过量碘导致的小鼠甲状腺氧化/抗氧化水平失衡、TPO活性水平下降都有有效的干预作用。     

Effects of selenium supplementation on hepatocarcinogenesis in rats

Four groups of weanling male Wistar rats (Groups A-D) received diethylnitrosamine (DEN, 40 ppm) in their drinking water for four weeks; after a recovery period of two weeks, they received (for the rest of the experiment) phenobarbital (PB, 500 ppm) added to a Torula yeast-based diet containing 0.17 ppm of selenium. Dietary selenium (2 ppm), as sodium selenite, was given to Group B one week before and during DEN treatment, to Group C one week before and during PB treatment, and to Group D during the entire experiment. Groups A and E received the unsupplemented diet, whereas Group E was not treated with DEN or PB. Pair-feeding conditions were used to minimize possible influences of differences in food intake and growth. Rats were killed at the 19th and 24th weeks after the experiment began. No significant differences were found in food and fluid intakes or in growth rates among the groups. Livers in Group E were histologically normal, whereas preneoplastic and neoplastic lesions were found in all other groups. In rats killed at the 19th and 24th weeks, the numerical and the volumetric densities of preneoplastic lesions did not differ significantly between all the groups. Similarly, the incidence of hepatocellular carcinomas only detected at 24 weeks was not significantly different between the groups. These results indicated that in this particular model of hepatocarcinogenesis, the dietary supplementation of 2 ppm of selenium did not modify the development of preneoplasia and carcinomas.     

Effect of dietary selenium on the induction of altered hepatic foci and hepatic tumors by the peroxisome proliferator ciprofibrate

The purpose of this study was to determine if the dietary antioxidant selenium could inhibit hepatocarcinogenesis induced by peroxisome proliferators, which are hypothesized to induce tumors by increased production of hydrogen peroxide or other reactive oxygen species. Rats were fed diets containing the peroxisome proliferator ciprofibrate and one of three concentrations (0.04, 0.2, or 1.0 ppm) of selenium for 6 or 21 months. The incidence of hepatic tumors and the number and volume of gamma-glutamyl transpeptidase-positive, ATPase-negative, glucose-6-phosphatase-negative, and glucose-6-phosphatase-positive foci at 21 months were lower in rats fed higher levels of selenium (no foci or tumors were seen at 6 mo). Indices of oxidative damage in the liver (thiobarbituric acid reactants, conjugated dienes, and lipid-soluble fluorescence products), however, were not decreased in rats fed the high-selenium diet. Therefore, selenium was protective against ciprofibrate-induced hepatocarcinogenesis, but not by reducing the degree of oxidative damage. The liver selenium and glutathione concentrations, and liver selenium-dependent glutathione peroxidase activity, increased as dietary selenium increased. Therefore, inhibition of carcinogenesis by selenium was correlated with increased levels of glutathione and glutathione peroxidase, but these did not inhibit the indices of oxidative damage. Peroxisomal beta-oxidation also increased with the dietary selenium content; it therefore does not appear to be a factor in the inhibition of hepatocarcinogenesis in rats fed higher levels of selenium.     

Effect of dietary selenium on the induction of altered hepatic foci and hepatic tumors by the peroxisome proliferator ciprofibrate

The purpose of this study was to determine if the dietary antioxidant selenium could inhibit hepatocarcinogenesis induced by peroxisome proliferators, which are hypothesized to induce tumors by increased production of hydrogen peroxide or other reactive oxygen species. Rats were fed diets containing the peroxisome proliferator ciprofibrate and one of three concentrations (0.04, 0.2, or 1.0 ppm) of selenium for 6 or 21 months. The incidence of hepatic tumors and the number and volume of γ‐glutamyl transpeptidase‐positive, A TPase‐negative, glucose‐6‐phosphatase‐negative, and gtucose‐6‐phosphatase‐positivefoci at 21 months were lower in rats fed higher levels of selenium (no foci or tumors were seen at 6 mo). Indices of oxidative damage in the liver (thiobarbituric acid reactants, conjugated dienes, and lipid‐soluble fluorescence products), however, were not decreased in rats fed the high‐selenium diet. Therefore, selenium was protective against ciprofibrate‐induced hepatocarcinogenesis, but not by reducing the degree of oxidative damage. The liver selenium and glutathione concentrations, and liver selenium‐dependent glutathione peroxidase activity, increased as dietary selenium increased. Therefore, inhibition of carcinogenesis by selenium was correlated with increased levels of glutathione and glutathione peroxidase, but these did not inhibit the indices of oxidative damage. Peroxisomal ß‐oxidation also increased with the dietary selenium content; it therefore does not appear to be a factor in the inhibition of hepatocarcinogenesis in rats fed higher levels of selenium.     

Effects of selenium supplementation on hepatocarcinogenesis in rats

Four groups of weanling male Wistar rats (Groups A—D) received diethylnitrosamine (DEN, 40 ppm) in their drinking water for four weeks; after a recovery period of two weeks, they received (for the rest of the experiment) phenobarbital (PB, 500 ppm) added to a Torula yeast‐based diet containing 0.17 ppm of selenium. Dietary selenium (2 ppm), as sodium selenite, was given to Group B one week before and during DEN treatment, to Group C one week before and during PB treatment, and to Group D during the entire experiment. Groups A and E received the unsupplemented diet, whereas Group E was not treated with DEN or PB. Pair‐feeding conditions were used to minimize possible influences of differences in food intake and growth. Rats were killed at the 19th and 24th weeks after the experiment began. No significant differences were found in food and fluid intakes or in growth rates among the groups. Livers in Group E were histologically normal, whereas preneoplastic and neoplastic lesions were found in all other groups. In rats killed at the 19th and 24th weeks, the numerical and the volumetric densities of preneoplastic lesions did not differ significantly between all the groups. Similarly, the incidence of hepatocellular carcinomas only detected at 24 weeks was not significantly different between the groups. These results indicated that in this particular model of hepatocarcinogenesis, the dietary supplementation of 2 ppm of selenium did not modify the development of preneoplasia and carcinomas.     

A buckwheat protein product suppresses gallstone formation and plasma cholesterol more strongly than soy protein isolate in hamsters

This study was conducted to investigate the effects of a buckwheat protein product (BWP) on plasma cholesterol, gallbladder bile composition and fecal steroid excretion in hamsters fed diets with 5 g/kg cholesterol. Diets also contained 200 g/kg of casein, soy protein isolate (SPI) or BWP as protein sources. After 2 wk, plasma and liver concentrations of cholesterol in the hamsters fed BWP were significantly lower than those in the hamsters fed casein and SPI. The molar proportion of cholesterol in gallbladder bile was significantly lower in the BWP group than in the other groups, whereas that of bile acids was slightly higher in the BWP group (P 相似文献   

Lack of effect of selenium on induction of tumors of esophagus and bladder in rats by two nitrosamines

The effect of differences in level of dietary selenium on the induction of esophageal and bladder tumors in rats by two nitrosamines was investigated. Groups of 20 female F344 rats were given a synthetic diet containing less than 0.05 ppm Se to which selenium (as sodium selenite) was added at the concentration of 0.35, 0.7, 1.4 and 2.1 ppm selenium. These four groups, plus one without added Se, were treated with 20 ml per rat per day, 5 days a week, of a solution of nitrosomethylcyclohexylamine containing 5 mg/liter. A parallel five groups were treated in the same way with a solution of nitrosomethyl-3-carboxypropylamine in drinking water containing 600 mg per liter, as drinking water. Treatment lasted 28 weeks, at which time some animals had developed tumors. A group of 20 rats fed 0, 1.4 and 2.1 ppm Se was not treated with carcinogen. Rats consuming 1.4 ppm or 2.1 ppm Se gained weight more slowly than other groups. There was no significant difference in survival between the five groups treated with each carcinogen but receiving different dietary levels of selenium. Neither was there any significant difference between groups receiving each carcinogen in the incidence of tumors of the esophagus induced by nitrosomethylcyclohexylamine or of tumors of the urinary bladder induced by nitrosomethylcarboxypropylamine. Control rats on the synthetic diets did not survive as well as untreated rats eating regular chow diet. In these conditions there was no effect of dietary selenium levels on the induction of tumors in female rats by the two carcinogenic nitrosamines we used.     

不同硒水平饲料对大鼠肝脏谷胱甘肽过氧化物酶和脱碘酶活性的影响

为了解不同饲料硒水平对大鼠肝脏中谷胱甘肽过氧化物酶和脱碘酶活性的影响及确定它们发挥最佳活性时的最低饲料硒水平。５４只体重为５０～６０ｇ的雄性断孔Ｗｉｓｔａｒ大鼠分成９组，分别喂以９种含硒水平为０．０１，０．０２，０．０３，０．０４，０．０５，０．０６，０．１，０．２和５ｍｇ／ｋｇ的不同饲料。实验持续２０周。９组动物２０周的体重增长除５ｍｇ／ｋｇ饲料组与０．１、０．２ｍｇ／ｋｇ饲料组之间有差异外，其余均没有显著性差异。谷胱甘肽过氧化物酶的活性随着饲料硒水平的升高而升高，当饲料硒含量为０．１，０．２和５ｍｇ／ｋｇ饲料时，活性达到最高。因此它发挥正常活性范围的最低饲料硒需要量为０．１ｍｇ／ｋｇ。９个组脱碘酶的活性（ｎｍｏｌ／ｍｉｎ．ｇ）在０．０５至０．２ｍｇ／ｋｇ饲料时活性最高，在５ｍｇ／ｋｇ饲料时酶活性降低，发挥最佳活性最低饲料硒需要量为０．０５ｍｇ／ｋｇ。     

Chronic inhalation of asbestos and cigarette smoke by hamsters.

One hundred and two male Syrian golden hamsters received chronic exposures to a respirable aerosol of Canadian chrysotile asbestos (mean aerosol concentration = 23 μg/l) 7 hours per day, 5 days per week. Half of the animals were also exposed for 10 minutes to cigarette smoke in modified Hamburg II smoking machines, three times per day, 5 days per week, for the duration of their life span. The other half of the animals received sham-smoke exposures. Another group of 102 hamsters served as controls. Half of the controls received smoke exposures, the other half received sham exposures. Asbestos exposure resulted in earlier and more severe lung lesions than in identical groups of concurrent experiments, which had received life span exposures to aerosols of NiO (53 μg/l) and CoO (10 μg/l), or which were treated with diethylnitrosamine (12 × 0.25 mg by s.c. injection). Asbestosis developed in all animals and forced discontinuation of the asbestos exposures after 11 months. Of 12 lung adenomas found in 510 hamsters, ten occurred among the 102 animals of the asbestosexposed groups, indicating an early neoplastic response. However, perhaps on account of their significantly shorter life span due to asbestosis, the incidence of laryngeal lesions and of malignant tumors wassignificantly lower in the asbestos + smoke-exposed group than in the control group having received smoke exposures. Neither a carcinogenic effect of asbestos nor a cocarcinogenic effect of cigarette smoke was observed. Cigarette smoke inhalation resulted in significantly lower mean body weights of the smoke-exposed groups.