Variation of the level of mercury and metallothionein in the kidneys and liver of rats with time of exposure to sodium selenite

Sodium selenite was administered to rats before, after, and simultaneously with mercuric chloride. In all animal groups, mercury was administered intravenously in doses of 0.5 mg/kg every other day for two weeks. Selenium was given intragastrically either in a single dose of 7.0 mg Se/kg or in repeated doses of 0.1 mg Se/kg every day for weeks. It was demonstrated that, depending on the administration schedule, selenium induced significant changes in the binding of mercury by soluble fraction proteins both in the kidneys and in the liver. In every exposure, the mercury content decreased mainly in the low-molecular weight proteins, and the level of metallothionein-like proteins was diminished in the both organs. In the kidneys, the mercury content showed a correlation with the level of metallothionein (r=0.78). Amounts of mercury below 10 μg/g kidney do not stimulate metallothionein biosynthesis in this organ. A distinct interaction effect was observed in the case of a simultaneous administration of equimolar amounts of both the metals in question.     

Effects of different selenium sources on tissue selenium concentrations,blood GSH-Px activities and plasma interleukin levels in finishing lambs

Thirty-two wether lambs of Tan sheep were randomly assigned into four dietary treatment groups (eight per group) for an 8-wk study and then fed a basal diet deficient in Se (0.06 mg/kg) or diets supplemented to provide 0.10 mg/kg Se from sodium selenite, selenized yeast, and selenium-enriched probiotics, respectively. Blood samples were collected at d 0, 28, and 56 of the experiment and tissue samples were collected at experiment termination. Tissue and blood Se concentrations, blood glutathione peroxidase (GSH-Px) activities, and plasma interleukin levels were analyzed. The results showed that the concentrations of Se in the kidney, liver, and muscle increased in all of the supplemented groups (p<0.01) compared with the control group. However, the Se concentrations in the kidney, liver, and muscle in the groups supplemented with Se yeast and Se-enriched probiotics were higher than those in the group supplemented with sodium selenite (p<0.01). The activities of GSH-Px and the concentrations of Se in blood also increased in all of the supplemented groups during the period of supplementation (p<0.01) compared with the control group. The activities of GSH-Px and the concentrations of Se in the whole blood of the lambs fed with selenized yeast and Se-enriched probiotics were higher than those of lambs fed with sodium selenite (p<0.01 or p<0.05). The concentrations of interleukin-1 and interleukin-2 in plasma significantly increased in all of the supplemented groups during the entire period of experiment (p<0.01) compared with the control group, but had no significant differences among all of the supplemented groups. In conclusion, a diet supplemented with Se for finishing lambs was able to increase the concentrations of Se in tissue and blood, activities of GSH-Px in blood, and levels of interleukins in plasma. Organic Se sources (selenized yeast and Se-enriched probiotics) were more effective than the inorganic Se source (sodium selenite) in increasing tissue and blood Se concentrations and blood GSH-Px activities of lambs. However, there were no significant differences in plasma interleukin levels of lambs between organic and inorganic Se sources.     

The effect of selenium and vitamin E on microvascular permeability of rat organs

The effects of dietary sodium selenite and vitamin E on the microvascular permeability of rat organs such as heart, brain, kidney, liver and eye were investigated by using the Evans blue leakage method. Combined deficiency of selenium and vitamin E caused an increase in the permeability of the heart and eye with respect to their controls while it had no considerable effect on the permeability of other organs. On the other hand, toxic levels of selenium (4.2 mg/kg) in diet decreased the permeabilities in kidney, liver, and eye whereas this parameter of brain increased in the same animal group. These results suggested that low or high sodium selenite and vitamin E contents in diet could alter the microvascular permeability of different organs in different manners. It might be important to give reasonable explanations for the pathophysiology of some diseases that are characterized with organ damage and /or disfunction originated from selenium deficiency or toxicity.     

The differential modulation of the enzymes of glutathione metabolism

The effect of methylmercury (MM) and MM plus sodium selenite (SE) on the activity of various GSH-dependent enzymes was studied in the liver and kidney of mice. Ten groups of mice were fed diets containing graded proportions of MM, alone or with graded quantities of SE. GST, GSH-Px, and GSSG-RED were assayed in the cytosolic fraction of liver and kidney homogenates. After treatment with MM, instead of the expected decrease in enzyme activities, an increase was observed in the kidney and a small decrease in the liver with no dose-response relation in either organ. In protected groups, a general pattern of induction was observed in both organs, but again there was little evidence of dose-response relationships. Detailed analysis of the results suggests that the effects observed were not directly caused by MM or SE but are the resultant of complex interactions presumably related to contemporaneous mechanisms of damage and repair.     

氟中毒大鼠肝肾自由基代谢及硒对其影响

为探讨硒对氟中毒大鼠肝、肾自由基代谢的影响,两组Wistar大鼠饮1.58 mmol/L和2.63 mmol/L高氟水;饮高氟水的同时加饲2.0 mg/kg硒饲料;饮氟水7个月后加饲硒饲料.实验14个月时用低温电子自旋共振(ESR)技术测其肝、肾活性氧自由基(FR)含量;同时测氟(F)、硒(Se)含量;谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性和脂质过氧化物(LPO)含量.结果：氟中毒大鼠在肝、肾氟升高的同时,FR和LPO上升,GSH-Px、SOD下降.在氟中毒不同时期投硒,大鼠肝、肾氟降低,FR和LPO减少,抗氧化酶活性恢复.表明硒不但可拮抗大鼠体内的高氟,还可纠正高氟造成的自由基代谢紊乱.     

Induction of metallothionein in rat tissues following subchronic exposure to mercury shown by radioimmunoassay

Although the analysis of metallothionein (MT) by radioimmunoassay (RIA) is not a common technique, its use is preferred over other methods since it offers the advantages of sensitivity and specificity. In this paper we present data on the basal levels of MT in rat tissues and physiological fluids of female Sprague-Dawley rats. The mean basal MT concentrations of the following organs and fluids were determined by RIA to be: liver (9.8 μg/g), kidney (68 μ/g), brain (0.8 μg/g), spleen (1.0 μg/g), heart (5.4 μg/g), plasma (11 ng/ml), and urine (200–300 μg/g creatinine). Following subcutaneous exposure to inorganic mercury (0.2 μmol/kg/d, 5 d a week for up to 4 wk), the metal accumulated primarily in the kidney. There was also a simultaneous accumulation of zinc in the liver and of zinc and copper in the kidney. Induction of MT did take place in liver, kidney, brain, and spleen. No increases in the MT contents of blood and urine were noted. The excess zinc and copper in the kidney of exposed animals were found to be associated predominantly with MT. No overt signs of mercury toxicity were noted in these animals and the incidence of proteinurea was nil. The data are discussed with reference to methods of MT determination in animal tissues and in relation to mercury metabolism and toxicity.     

Effect of dietary fluoride on selenite toxicity in the rat

Three factorial experiments were conducted to determine if high dietary fluoride (F) would inhibit selenite toxicity in rats. Initially, three levels of selenite (0.05, 3, and 5 mg/kg diet) were matched against three levels of F (2, 75, and 150 mg/kg diet). Fluoride failed to prevent the depressive effect of selenite on 8-wk food intake and body wt gain. Selenium (Se) concentration of plasma and kidney and enzymatic activity of whole blood glutathione peroxidase (GSH-Px) were also unaffected by F. Liver Se concentration, however, was slightly (12%) but significantly (p<0.025) reduced when the highest F and Se levels were combined. Fluoride (150 mg/kg) appeared to reduce liver selenite toxicity (5 mg/kg). Therefore, further study focused on liver histology with treatments that eliminated the middle levels of selenite and F. Fluoride prevented the hepatic necrosis seen in selenite-toxic rats. Similar histological lesions were not observed for kidney or heart. Fluoride partially (26%) but significantly (p<0.025) reduced thiobarbituric-reactive substances in selenite-toxic rats, but there was no F effect on intracellular distribution of liver Se, glutathione levels in liver and kidney, or on liver xanthine oxidase activity. Overall, the protective effect of F on selenite toxicity appears to be confined to liver pathology. The exact mechanism for this effect, however, remains unclear. Oregon Agricultural Experiment Station Technical Paper No. 9728.     

Effects of glutathione and of cysteine on intestinal absorption of selenium from selenite

The influence of glutathione (1 mmol/L) (GSH) on in vitro mucosal uptake and in vivo absorption of⁷⁵Se-labeled selenite (10 μmol/L) was investigated in rat jejunum. For comparison, the effect ofl-cysteine (1 mmol/L) on in vivo absorption of⁷⁵Se-labeled selenite was also studied. In the in vitro, uptake experiments, only the mucosal surface was exposed to the incubation medium for 3 min. For the in vivo experiments, a luminal perfusion technique was employed. GSH inhibited in vitro mucosal Se uptake, whereas absorption in vivo was stimulated by GSH.l-Cysteine also stimulated in vivo Se absorption, confirming former in vitro mucosal uptake experiments. Thus, unlikel-cysteine, GSH affected in vitro and in vivo absorption of Se from selenite differently. Enzymatic cleavage of products of the reaction of selenite with GSH occuring more efficiently under in vivo than in vitro conditions may be a prerequisite for the stimulatory effect of GSH on Se absorption. This apparently does not apply to the stimulatory effect of cysteine. Since, GSH occurs in the intestinal lumen under physiological conditions, it may contribute to the high bioavailability of Se from selenite.     

The potential protective role of folic acid against acetaminophen-induced hepatotoxicity and nephrotoxicity in rats

Folic acid (FA), is a group B vitamin, has high reactive oxygen radicals quenching ability, resulting in protection against oxidative damage in aerobic cell. Acetaminophen (N-acetyl-p-aminophenol, APAP) is a nonsteroidal anti-inflammatory drug, and can promote oxidative damage in liver and kidney tissues. The aim of this study was to investigate whether folic acid has protective effects on oxidative liver and kidney injury caused by experimental APAP toxication. Forty female Sprague dawley rats were divided into 5 groups; control, APAP, FA, APAP+FA, and APAP+N-acetylcysteine (NAC) groups. APAP toxication was induced by oral gavage (3 g/kg bodyweight). FA (20 mg/kg bodyweight) and NAC (150 mg/kg bodyweight) were given by oral gavage to the specified groups. Oxidant and antioxidant parameter were determined in liver and kidney tissues. In addition, the liver and kidney tissues were histological evaluated. When compared with APAP group, superoxide dismutase (SOD) and catalase activities and glutathione levels were statistically higher, malondialdehyde (MDA) level and myeloperoxidase activity (except liver tissue) were statistically lower in both APAP+FA and APAP+NAC. Liver and kidney MDA level and kidney SOD activity were significantly lower in APAP+NAC group compared with APAP+FA group. Co-administration of NAC with APAP was found to provide protection, but hepatic cords were defective in some places and some glomerular tubules also had dilatation. Necrotic areas was reduced in the liver and the glomerular structure was in good condition in the APAP+FA group. As a result, FA might have a protective effect against APAP-induced hepato-nephrotoxicity and oxidative stress in rat.     

箬叶多糖及其化学修饰物、亚硒酸钠和GSH对Cu~(2+)诱导的LDL氧化修饰的保护作用

研究了箬叶多糖ＦⅢ－ａ及其化学修饰物、亚硒酸钠和ＧＳＨ对Ｃｕ２＋诱导的低密度脂蛋白氧化修饰的保护作用．其结果表明箬叶多糖、硫酸酯多糖、硒酸酯多糖可显著抑制脂质过氧化产物（ＴＢＡＲＳ）及荧光物质的生成,彼此之间无明显差异．但对ＶＥ的消耗有着不同的保护作用,其顺序是ＦⅢ－ａ＞Ｓ－ＦⅢ－ａ＞Ｓｅ－ＦⅢ－ａ,并且具有明显的量效关系．硒或ＧＳＨ对Ｃｕ２＋诱导的ＬＤＬ氧化修饰无明显的抑制,但联合使用在０．１２５ｍｍｏｌ／ＬＮａ２ＳｅＯ３和０．２ｍｍｏｌ／ＬＧＳＨ及１２．５μｍｏｌ／ＬＮａ２ＳｅＯ３和０．０２ｍｍｏｌ／ＬＧＳＨ的浓度下能强烈地抑制ＴＢＡＲＳ的生成,甚至比正常的ＬＤＬ还要低．但是对ＶＥ的消耗只有较弱的保护作用,硒酸酯多糖与此相似．Ｎａ２ＳｅＯ３在０．１２５ｍｍｏｌ／Ｌ时可以明显抑制荧光物质的生成．     

东北红豆杉细胞培养生产紫杉醇的调控研究

研究了诱导子、前体及抑制剂的协调作用对东北红平杉生产紫杉醇的影响。结果表明,向培养基中加入80mg/L水到、80mg/L茉莉酸甲酯、0.5mmol/L乙酸钠、2mmol/L苯丙氨酸、0.5mmol/L丝氨酸、0.1mmol/L甘氨酸、10mg/L肉桂酸、0.5mmol/L苯甲酸钠、5mmol/L丙酮酸钠、10mg/L氯化氯胆碱、和1mg/L赤霉酸可使紫杉醇含量提高368.65%。并且证明交互作用对紫杉醇合成有显著作用。     

Effect of fertilization on selenium content of tea and the nutritional function of Se-enriched tea in rats

The present study examined the effect of fertilization with sodium selenite on the selenium content of tea and the nutritional function of Se-enriched tea. Selenium content of tea leaves was increased up to 0.36 g g^–1 by the application of sodium selenite to soil at 0.5 and 1.0 kg Se ha^–1. Application by a Se-enriched organic manure at a rate of 0.5 kg Se ha^–1 provided a higher biological availability of selenium for plant uptake compared with a similar amount of sodium selenite. Foliar spray of sodium selenite at 50–100 g Se ha^–1 increased the selenium content to 0.32–1.45 g g^–1 in tea leaves sampled at the 8–26 days after spraying. Selenium content in the blood and liver, glutathione peroxidase activity in blood of rats were significantly enhanced by feeding of an extracted solution of Se-enriched tea leaves and sodium selenite. Glutathione peroxidase activity in liver of rats fed with Se-enriched tea was higher than that fed with sodium selenite, indicating that the selenium in Se-enriched tea leaves is a more effective Se source than sodium selenite. Increasing the Se level in food products through the application of a selenium fertilizer is a safe, effective and feasible means of increasing the selenium intake of human and animals in low selenium areas of China.     

Selenium supplementation of infant formula: uptake and retention of various forms of selenium in suckling rats

Formula-fed infants often have lower serum selenium levels than breast-fed infants. Although no deleterious effects have been correlated to this finding, supplementation of formula with selenium is considered. In this study, we investigated the uptake and retention by suckling rat pups of ⁷⁵Se from selenite, selenate, and selenomethionine added to infant formula. The molecular distribution of ⁷⁵Se in liver, kidney, intestine, and plasma was followed by gel-filtration chromatography on Superose 12. ⁷⁵Se-uptake was most rapid from selenomethionine (70% at 1 hr), followed by selenate (51%) and selenite (29%). This difference was explained by a higher retention of ⁷⁵Se in the stomach and small intestinal wall of pups given selenite supplement. Plasma distribution of ⁷⁵Se as studied by gel filtration was also different, with a higher proportion of ⁷⁵Se from selenomethionine being protein-bound than from selenite or selenate. Similarly, a larger proportion of ⁷⁵Se from selenomethionine became protein-bound in the liver than from selenite or selenate. In conclusion, although whole body retention after 24–48 hr was similar, the metabolic fate of selenium varies considerably with the form of selenium added to formula. Further studies are needed to study the long-term consequences of selenium accumulated in different body compartments.     

Differences in the growth inhibition of cultured K-562 cells by selenium, mercury or cadmium in two tissue culture media (RPMI-1640, Ham's F-10)

Effects of some metals on the growth of cultured human erythroleukemia K-562 cells were investigated when grown in two different types of media based upon RPMI-1640 or Ham's F-10. The study on proliferation, using RPMI-1640 supplemented with sodium selenite, selenomethionine, mercuric chloride, methylmercuric chloride and cadmium nitrate showed no inhibition of growth at concentrations of 2.5, 25, 25, 2.5 and 25 M, while at 75, 250, 50, 5 and 50 M toxicity was apparent. Selenite at 5–50 M and selenomethionine at 50–100 M inhibited the growth. In Ham's F-10 supplemented with the same compounds no inhibition was found at concentrations of 5, 10, 25, 1 and 50 M, while at 50, 100, 50, 5 and 75 M toxic effects were noted. Selenite 10 M and selenomethionine 25-50 M inhibited the proliferation. Measurements of trace element levels in pellets of K-562 cells grown in RPMI-1640 or Ham's F-10 unveiled higher cell contents of cadmium and selenium in cells grown in RPMI-1640, being consistent with higher concentrations of these elements in that medium. Manganese and mercury concentrations were higher in cells grown in Ham's F-10 correlating with a higher medium concentration of these elements. The growth responses and cellular uptake differed between the metals and the selenocompounds and although extrapolating the results to humans is difficult the selenium exposures were in approximately the same order of magnitude as in human exposures. The compounds could be ranked according to decreasing toxicity as: methylmercuric chloride > mercuric chloride, cadmium nitrate, sodium selenite > selenomethionine.     

Selenium in the anterior pituitary of the rat after a single injection of75Se sodium selenite

In order to investigate the selenite metabolism in the anterior pituitary and compare it with other endocrine organs, rats were injected intraperitoneally with⁷⁵Se sodium selenite (5 mg/kg). The rats were whole body counted shortly after injection and recounted just before sacrifice, which was performed 2, 24, 48 h, and 4, 10, 20, 30, 40, 60, and 80 d after injection. Besides the anterior pituitary, the selenium content was also estimated in the thyroid gland, testis, adrenals, liver, kidney, and blood. The maximum selenium content was observed in all organs 2 h after injection, at which time the anterior pituitary contained 2.9 μg/g wet wt, compared to 13.5 μ/g wet wt in liver and .6 μg/mg wet wt in testis. The excretion of selenite from the anterior pituitary resembled that seen in most other organs investigated, i.e., an initial rapid excretion and a slower secondary phase resembling a first order reaction. Practically all selenium was excreted by 60 d after injection.     

培养方式对富硒产朊假丝酵母性能的影响

在摇瓶和5 L发酵罐水平上分别考察亚硒酸钠浓度及其添加方式对高性能(高有机硒含量和高谷胱甘肽含量)富硒产朊假丝酵母制备的影响.结果表明:亚硒酸钠添加质量浓度为15 mg/L时,产朊假丝酵母具有较好的富硒效果,但一次性添加对酵母细胞有较大的毒害作用.采用分批次添加亚硒酸钠的方法获得了较好的制备高性能富硒产朊假丝酵母的培养方式:发酵起始添加L-蛋氨酸10 mmol/L,并在发酵过程的12和15 h分别添加亚硒酸钠10和5 mg/L.在此培养方式下,产朊假丝酵母胞内谷胱甘肽和有机硒含量分别达到172.3 mg/L和1194 μg/g.     

卫星灵芝液体发酵富集硒锌的研究

研究不同浓度的硒、锌对卫星灵芝菌丝体生长的影响,初步探讨卫星灵芝菌丝体生物富集硒、锌的效应。采用平板培养法及液体发酵法研究锌、硒对卫星灵芝菌丝体生长的影响及富集效应。培养基中不同浓度的亚硒酸钠对菌丝体生长均具有不同程度的抑制作用,但灵芝菌丝体的富硒量随着硒浓度的增加而提高,当亚硒酸钠浓度为40 mg/L时,菌丝体中的生物量、富硒量及富硒转化率最高,分别为1.54%、2 131.55 mg/kg、32.91%;培养基中硫酸锌浓度低于150 mg/L的范围内对卫星灵芝菌丝体生长有明显的促进作用,硫酸锌浓度为60 mg/L时菌丝体中的锌含量和富锌转化率最高,分别为1 142.91 mg/kg、1.76%。培养基中同时添加40 mg/L的亚硒酸钠和60 mg/L硫酸锌,菌丝体生长量1.60%,富硒量301.85 mg/kg,富硒率4.84%;富锌量为540.41 mg/kg,富锌率为5.72%。     

还原亚硒酸盐产生红色单质硒光合细菌菌株的筛选与鉴定

从实验室保藏的光合细菌中筛选出一株对亚硒酸钠还原效率较高的菌株S3,其亚硒酸钠还原产物通过透射电子显微镜及EDX(Electron-Dispersive X-ray)分析确定为红色单质硒。菌株S3的形态学特征、生理生化特征及光合色素扫描结果与固氮红细菌(Rhodobacter azotoformans)的特征基本一致;16S rDNA序列(GenBank登录号为DQ402051)在系统发育树中与固氮红细菌同属一个类群,序列同源性为99%。根据上述结果将菌株S3鉴定为固氮红细菌。初步研究了该菌株还原亚硒酸钠的特性,首次报道固氮红细菌具有还原亚硒酸盐产生红色单质硒的能力,为今后利用微生物方法治理环境中硒污染、利用微生物方法获得活性红色单质硒以及对微生物还原亚硒酸盐产生红色单质硒的机理研究奠定了良好的基础。     

Microencapsulated sodium selenite supplementation in dairy cows: effects on selenium status

The objective of this study was to compare the efficiency of transfer of selenium (Se) to plasma and milk from inorganic sodium selenite, either free or microencapsulated, and from selenized yeast in dairy cows. The study consisted of an in situ-nylon bags incubation, and in an in vivo experiment to compare the Se status of cows supplemented with either sodium selenite, microencapsulated sodium selenite, or Se yeast. Thirty dairy cows, divided in five groups, were fed the following diets: the control group (CTR) received a total mixed ration supplemented with sodium selenite in order to have 0.3 mg/kg DM of total Se; 0.3M and 0.5M groups received the same control diet supplemented with lipid microencapsulated sodium selenite to provide 0.3 and 0.5 mg/kg DM of total Se, respectively; 0.3Y and 0.5Y groups received selenized yeast to provide 0.3 and 0.5 mg/kg of total Se, respectively. Cows were fed the supplements for 56 days during which milk, blood, and fecal samples were collected weekly to conduct analysis of Se and glutathione peroxidase (GSH-px) activity. Se concentration in the nylon bags was assessed to 72%, 64%, and 40% of the initial value (time 0) after 4, 8, and 24 h of incubation, respectively. In vivo, cows supplemented with 0.3 mg/kg of microencapsulated Se had higher milk Se concentration compared to CTR. The increment was more pronounced at the highest inclusion rate (0.5 mg/kg, 0.5M group). GSH-px activity was not significantly affected by treatments. The results indicate that lipid microencapsulation has the potential to protect nutrients from complete rumen reduction and that Se from microencapsulated selenite is incorporated in milk more efficiently than the free form. Microencapsulated sodium selenite was shown to be comparable to Se-yeast in terms of availability and incorporation in milk when fed at 0.3 mg/kg DM, whereas the inclusion in the diet at 0.5 mg/kg DM resulted in higher plasma and milk concentrations than selenized yeast.     

Effect of selenium-enriched malt on hepatocarcinogenesis, paraneoplastic syndrome and the hormones regulating blood glucose in rats treated by diethylnitrosamine

233 SD rats weighing 100 approximately 120 g were divided randomly into 6 groups. The animals in group I and group II received 0.1 mg/kg selenium in the form of sodium selenite only and served as the negative control and positive control, respectively. Animals in groups III, IV and V were fed with selenium as Se-enriched malt supplemented diets (0.3, 1 and 3 mg/kg), and group VI with selenium by using sodium selenite supplemented diets (3 mg/kg). Animals of groups II approximately VI were induced hepatoma by diethylnitrosamine (100 mg/l) for 16 weeks, then drunk with sterilized water for 2 more weeks. Subsequently, the effects of Se-enriched malt and sodium selenite on hepatoma nodules, relative liver weight, the liver function indices including alanine aminotransferase (ALT), alkaline phosphatase (ALP), albumin (ALB), total bilirubin (TBIL), and the tumor markers, named as gamma-glutamyltranspeptidase (GGT), alpha-fetoprotein (AFP), insulin-like growth factor-II (IGF-II) were recorded. The calcium concentration, glucose content in plasma and values of the hormones regulating blood glucose, such as insulin, glucagons and thyroid hormones (3,5,3'-tetraiodothyronine, T(3); 3,5,3'5'-tetraiodothyronine, T(4)) were observed as well. At the same time, the correlations between the concentration of plasma glucose and related hormones were also analyzed. The results indicated that Se-enriched malt showed a better chemopreventive efficiency in decreasing the number of hepatoma nodules, relative liver weight and the contents of AFP, GGT, IGF-II, ALT, ALP and TBIL in the plasma, and delaying the descent of hormones in the serum, names as insulin, glucagons, T(3) and T(4) than those feeding with sodium selenite. Effect of Se-enriched malt excelled sodium selenite in the aspects of deadening the descent of glucose concentration in the plasma and the rise of calcium concentration in the serum of the rats with hepatoma induced by diethylnitrosamine. The values of glucose and calcium were significantly related to those items fore-named. In conclusion, the function of Se-enriched malt in deadening the lesion and delaying the development of hepatoma of rats induced by diethylnitrosamine was better than that of sodium selenite. Hypoglycemia and hypercalcemia were significantly correlated with the multifactors mentioned above.