The organ distribution of selenium in German adults

The selenium concentrations were determined in liver, kidney, skeletal muscle, heart, brain, prostate, testis, bile, lung, and spleen of German traffic accident victims. In addition the nitrogen and phosphorus contents were determined in the same organs and tissues. On a per-weight unit basis, the highest selenium concentration was found in kidney. However, this corresponds to only 4% of the total body selenium. Most of the whole body selenium (50%) is present in skeletal muscle, which thus appears to act as a selenium storage organ. However, there is also evidence that selenium is required for muscle function. In plasma and interstitial fluid, .450 mg of Se, or 7.5% of the total body selenium is present. A comparison of the organ Se concentrations of the German traffic accident victims with the selenium concentrations of the same human organs as reported in different countries indicates that the organ concentrations of West Germans are comparable to that of the population of New Zealand, a low-Se country, and significantly lower than that observed in the organs of American, Canadian, and especially Japanese subjects. The international comparison of the organ selenium concentrations also revealed that the selenium uptake of kidney is higher at low- and adequate dietary Se intakes and lower if the dietary Se supply is high, as is the case for Japanese subjects. Estimates of the daily excretion of selenium with the bile indicate that the amounts are three times higher than the daily urinary losses and in the same order of magnitude as the daily dietary selenium intakes. Enterohepatic reabsorption of selenium from the bile appears to be a significant mechanism of conserving dietary selenium and to maintain Se balance at comparatively low dietary Se intakes.     

Effect of dietary organic versus inorganic selenium in laying hens on the productivity, selenium distribution in egg and selenium content in blood, liver and kidney.

We investigated the effect of organic versus inorganic dietary selenium in laying hens on the productivity, selenium distribution in egg and selenium content in blood, liver and kidney. Sixty Leghorn laying hens were fed a basic diet containing 0.23mg Se/kg DM (dry matter) for 2 weeks and then were allocated randomly into three groups. Thereafter, the hens were given the same basic diet without supplementation, or with 0.51 mg Se/kg DM as sodium selenite (SS) or Se-malt (SM). During the experiment, egg rate and dietary intake were recorded, blood was sampled on days 10 and 20, and six eggs were sampled on days 8, 16 and 24 from each treatment group for Se content determination. At the end of the experiment, 10 hens from each treatment were slaughtered, and liver and kidney were sampled for the determination of Se content. The result showed that with the increase of dietary Se level, the Se content in egg, blood, liver and kidney was elevated (P < 0.05), but the hens' productivity was not affected. SS increased liver Se content more than SM (P < 0.05), while the Se content both in blood and kidney did not differ significantly between the SS and SM treatments. Se from SM and SS mainly deposited in the egg yolk. This suggests that the metabolic route of Se from SM is similar to that of Se from SS in laying hens.     

The bioavailability of various selenium compounds to a marine wading bird

The uptake of dietary selenium (about 3.5 mg/kg AF dry wt) as selenomethionine, selenocystine, selenite, selenate, and fish selenium in the plasma and red blood cells (RBC) of the oystercatcher has been investigated. The birds received the various selenium compounds subsequently, for at least 9 wk. After dietary supplementation of selenocystine, selenite, and selenate, plasma selenium was about 350 μg/L and RBC selenium 2.1 mg/kg dry wt. After supplementation of selenomethionine, the plasma concentration increased to 630 μg/L, and the RBC concentration to 4.1 mg/kg dry wt. When the fodder contained 3.1 mg/kg fish Se, an average plasma and RBC concentration of 415 μg/L and 14.4 mg/kg dry wt, respectively, was measured. The maximal increase of the selenium concentration in the plasma was attained at first sampling, 14 d after a change in dietary selenium (selenomethione or fish Se); the uptake seemed to be a concentration-regulated process. RBC concentrations (γ in mg/kg dry wt) increased with time (X in d) according toY=a?be^?cX . Fifty percent of the total increase was attained within 17d, suggesting that diffusion into the RBC played a role. The selenium concentration in the plasma was positively correlated with the (fish) Se concentration in the fodder; the RBC concentration (60 d after the change in diet) was positively correlated with the plasma concentration. When the diet contained fish Se, the blood selenium concentrations of the captive birds were similar to the concentrations measured in field birds. Fish Se is a yet undetermined selenium compound. The present experiment showed that fish Se differed from selenomethionine, selenocystine, selenite, or selenate in uptake from the food and uptake in the RBC.     

Effect of dietary selenium concentration and duration of selenium feeding on hepatic glutathione concentrations in rats

Studies were conducted in rats to determine the effect of dietary selenium (Se) concentration on hepatic glutathione concentrations and enzyme activities associated with the maintenance of the cellular glutathione status. Male rats were fed 0.1, 3.0, or 6.0 ppm Se as Na2SeO3 for 2, 4, or 6 weeks at which time they were killed and analyses were performed. Both 3.0 and 6.0 ppm Se caused a significant dose-dependent increase in hepatic-reduced glutathione (GSH) by 4 weeks of feeding compared to 0.1 ppm Se. The increase in GSH was preceded by significant, dose-dependent increases in oxidized glutathione (GSSG) as well as the GSSG to GSH ratio. Increases in GSSG and the GSSG to GSH ratio as well as in glutathione reductase and glucose-6-phosphate dehydrogenase activities were observed by 2 weeks of high Se feeding. The current findings substantiate previous results demonstrating effects of high Se on hepatic glutathione concentrations (R. A. LeBoeuf and W. G. Hoekstra, J. Nutr. 113:845-854, 1983) and further suggest that increased cellular GSSG concentrations or the GSSG to GSH ratio caused by 3.0 and 6.0 ppm dietary Se signals for "adaptive" changes in hepatic glutathione metabolism.     

Gestational changes in concentrations of selenium and zinc in the porcine fetus and the effects of maternal intake of selenium

The effect of maternal dietary selenium (Se) and gestation on the concentrations of Se and zinc (Zn) in the porcine fetus were determined. Mature gilts were randomly assigned to treatments of either adequate (0.39 ppm Se) or low (0.05 ppm Se) dietary Se. Gilts were bred and fetuses were collected throughout gestation. Concentrations of Se in maternal whole blood and liver decreased during gestation in sows fed the low-Se diet compared to sows fed the Se-supplemented diet. Maternal intake of Se did not affect the concentration of Se in the whole fetus; however, the concentration of Se in fetal liver was decreased in fetuses of sows fed the low-Se diet. Although fetal liver Se decreased in both treatments as gestation progressed, the decrease was greater in liver of fetuses from sows fed the low-Se diet. Dietary Se did not affect concentrations of Zn in maternal whole blood or liver or in the whole fetus and fetal liver. The concentration of Se in fetal liver was lower but the concentration of Zn was greater than in maternal liver when sows were fed the adequate Se diet. These results indicate that maternal intake of Se affects fetal liver Se and newborn piglets have lower liver Se concentrations compared to their dams, regardless of the Se intake of sows during gestation. Thus, the piglet is more susceptible Se deficiency than the sow.     

The influence of dietary selenium and vitamin E on glutathione peroxidase and glutathione in the rat

The effect of dietary selenium (Se) and vitamin E supplementation on tissue reduced glutathione (GSH) and glutathione peroxidase activity has been studied in the rat. Increasing Se intake by 0.4 ppm gave significantly higher enzyme levels in all tissues studied, an effect not influenced by vitamin E intake. Further increasing Se to 4 ppm gave higher enzyme levels in red blood cells only, while in liver was there was a significant decrease in enzyme activity probably reflecting Se hepatotoxicity. In the absence of Se supplements increasing dietary vitamin E to 100 mg/kg diet significantly increased enzyme activity but this effect was modified by simultaneous Se supplementation.Se intake had no effect on GSH levels. Rats on high vitamin E intake 500 mg/kg had a significantly higher tissue GSH level. Dietary Se had a sparing effect on vitamin E, rats supplemented with Se having significantly raised plasma vitamin E levels.These results confirm the role of selenium in glutathione peroxidase and also show that vitamin E influences the activity of the enzyme.     

Dietary selenium levels modulates antioxidant,cytokine and immune response and selenoproteins mRNA expression in rats under heat stress condition

BackgroundHigher environmental temperature is a major abiotic stress factor for animals and human beings. The selenium (Se) is an important trace mineral having diverse health promoting effects under stress conditions. However, studies on dietary requirement of selenium under prolonged heat stress condition are lacking. Present study discern the effect of higher dietary Se levels on antioxidant, cytokine, haemato-biochemical profile, and immune response, and the selenoproteins mRNA expression in rats under prolonged heat stress (HS) condition.MethodsWeaned Wistar rats (4 wk age; 67.6 ± 1.53 g BW; n = 72) housed under thermoneutral (TN) or HS conditions and fed with purified diets containing three graded Se levels were divided in six experimental groups. The groups were 1) TN control with 138 ppb Se (TN_CON), 2) HS control with 138 ppb Se (HS_CON), 3) TN with higher Se @ 291 ppb (TN_Se1), 4) HS with higher Se @ 291 ppb (HS_Se1) 5) TN with higher Se @ 460 ppb (TN_Se2), 6) HS with higher Se @ 460 ppb (HS_Se2). Rats in all the six groups were maintained in TN environmental conditions (57.3 ± 0.22 temperature humidity index; THI) for initial 28 days period. Subsequently, rats of HS groups were exposed to 77.0 ± 0.11 THI for 6 h/d in a psychrometric chamber for last fourteen days.ResultsHigher dietary Se (291 and 460 ppb) significantly improved the blood hemoglobin concentration and reduced serum alanine aminotransferase activity of rats under HS conditions. The serum triiodothyronine and insulin levels were significantly higher in high dietary Se groups irrespective of the environmental conditions. Similarly, the serum reduced glutathione levels, and catalase and superoxide dismutase enzyme activity were increased and malondialdehyde levels were reduced in high dietary Se groups irrespective of stress conditions. The glutathione peroxidase (GPx) activity was significantly higher in 460 ppb dietary Se groups as compared to other groups. The serum pro-inflammatory cytokine interleukin (IL)− 1 was declined, whereas the anti-inflammatory cytokine IL-10 level was increased in high dietary Se fed rats under both HS and TN conditions with 460 ppb dietary Se groups showing pronounced effects. Further, there was heat stress- and dietary Se level dependent- up regulation in hepatic GPx and iodothyronine deiodinase-II mRNA expression and similar pattern was noticed in hepatic thioredoxin reductase mRNA expression. The selenoprotein-P mRNA expression was up regulated in 460 ppb Se fed HS group as compared to CON and Se1_C groups. High dietary Se improved the humoral immune response 7d after antigen inoculation under HS conditions whereas cell-mediated immune response was augmented in rats fed higher Se under TN condition.ConclusionIt is concluded that under prolonged heat stress conditions the dietary requirement of Se may be increased to 460 ppb for improving the antioxidant status and humoral immune response, cytokine levels, modulating the thyroid and insulin hormone, and the selenoproteins mRNA expression of rats.     

Dietary selenium supplementation prolongs pentobarbital induced hypnosis

The present studies characterized the influence of dietary selenium (Na2SeO3) on the duration of pentobarbital (PB) induced hypnosis (sleep) in the rat. Rats were fed semipurified diets varying from 0.01 to 2.0 mg Se/kg for up to 4 weeks. Consumption of diets containing 1.0 and 2.0 mg Se/kg significantly prolonged PB induced hypnosis. Hepatic selenium, but not hepatic glutathione peroxidase activity, correlated with the length of PB induced hypnosis. The prolongation of hypnosis caused by diets containing 1.0 mg Se/kg was substantially reduced or eliminated by repeated exposure to PB. Although single exposure to increasing quantities of PB (60-100 mg/kg body weight) led to a progressive increase in sleep duration, the proportional increase caused by supplemental selenium (2.0 vs 0.1 microg Se/g) remained relatively constant (approximately 25%). Increasing maturity was inversely related to the duration of PB induced hypnosis, regardless of dietary selenium provided. Consumption of the 2.0 mg Se/kg diet prolonged PB induced hypnosis to a greater degree in immature than in mature rats (P < 0.05). Consumption of the selenium enriched diet (2 microg Se/g) resulted in an increase in cytochrome 2B, but had no effect on cytochrome 1A compared to controls (0.1 microg Se/g). Pretreatment of rats with P450 enzymes activators (i.e., PB, Aroclor 1254, or 3-methylcholanthrene) shortened the duration of PB induced sleep and masked the effects of dietary selenium. The current studies document that dietary selenium can influence the response to pentobarbital induced hypnosis and likely relates to changes in drug detoxification enzymes.     

Different bioavailability in humans of wheat and fish selenium as measured by blood platelet response to increased dietary Se

The bioavailabilities of selenium (Se) from Se-rich fish species and Se-rich wheat were compared in a study involving 32 healthy volunteers. Initial serum Se values were 109±16 μg/L (mean±SD). For 6 wk, one group (n=11) included Se-rich bread in their diet, bringing daily average intake of Se up to 135±25 μg/d. Another group (n=11) consumed Se-rich fish daily (average Se intake: 115±31 μg/d), whereas the control group (n=10) ate their normal diet, providing 77±25 μg Se/d. Serum Se increased by 17% (P<0.01), and platelet Se increased by 30% (P<0.01) in the wheat group. Although platelet Se decreased by 11% in the fish group, no changes in serum and platelet Se in the fish or control group reached statistical significance. Glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity in serum and platelets did not change during the study, nor did platelet mercury (Hg) content. Since the dietary intake of Hg, arsenium (As), and fatty acids could not satisfactorily explain the lack of response in the fish group, the results are indicative of low bioavailability of fish Se in humans. At present, wheat Se seems to be the most important factor contributing to the body stores of Se in this study population. Dr. Norheim died on January 9, 1991.     

Colostrum and milk selenium,antioxidative capacity and immune status of dairy cows fed sodium selenite or selenium yeast

Dietary selenium (Se) can be supplemented from organic or inorganic sources and this may affect Se metabolism and functional outcome such as antioxidative status and immune functions in dairy cows. A feeding trial was performed with 16 Holstein-Friesian dairy cows fed with a total mixed ration (0.18 mg Se/kg dry matter (DM)) either without Se supplement (Control, n = 5), or with Se from sodium selenite (Group SeS, n = 5) or Se yeast (Group SeY, n = 6). In Groups SeS and SeY, the Se supplementation amounted to an additional intake of 4 mg Se and 6 mg Se/d during gestation and lactation, respectively. The effect of both Se sources was characterised by milk Se and antioxidant levels, and the phenotyping and functional assessment of phagocytic activity of milk immune cells. Se yeast has been found to increase (p ≤ 0.001) the milk Se and antioxidant levels markedly compared to the control group. The experimental treatment did not affect the immune parameters of the cows. Lymphocyte subpopulations and phagocytosis activity of neutrophilic granulocytes were affected neither by the Se intake nor by the two different dietary supplements. It can be concluded that sodium selenite and Se yeast differ considerably in their effects on antioxidant status in dairy cows. However, the basal dietary Se concentration of 0.18 mg/kg DM seemed to be high enough for the measured immune variables.     

Absorption, distribution, half-life and possible routes of elimination of dietary selenium in juvenile rainbow trout (Salmo gairdneri)

1. The influence of different levels of dietary selenium on the metabolism of selenium in rainbow trout was studied using 75Se as an indicator. 2. Gastric absorption of selenium by the trout appeared to be very efficient. 3. Highest tissue concentrations of selenium were noted in the liver and kidney. 4. Blood did not concentrate selenium and the plasma was the major transport medium. 5. The liver and kidney appeared to be involved in selenium excretion based on high tissue concentrations and variations in half-lives with selenium loading. 6. The biological half-life of selenium in the tissues decreased with increased selenium loading except in the liver, which at toxic dietary selenium concentrations became longer, suggesting a rate-limiting metabolic transformation of selenium for excretion in this organ.     

Relationship of dietary intake of fish and non-fish selenium to serum lipids in Japanese rural coastal community.

Several studies have suggested that dietary selenium deficiency may be associated with an increased risk of coronary heart disease (CHD). In the present study, 55 men and 71 women were selected from participants in a health examination in a rural coastal community in Japan. The mean dietary selenium intake calculated from the simple food frequency questionnaire (SFFQ) was 127.5 micrograms/day. Fish was the major source of dietary selenium and it contributed to 68.7% of the daily total. HDL cholesterol was higher in the middle selenium intake group and in the high selenium intake group than in the low selenium intake group in all subjects and for males, and a significant difference was found between the middle selenium intake group and the low selenium intake group. The atherogenic index was significantly higher in the low selenium intake group than in the middle selenium intake group and in the high selenium intake group in males. GPx activity, total cholesterol and triacylglycerols did not show any significant differences among the three different selenium intake groups. Dietary intake of non-fish Se had a positive correlation with HDL cholesterol, and an inverse correlation with the atherogenic index in all subjects and for females. On the other hand, dietary intake of fish-Se had no relationship with any serum lipids. Non-fish Se is an important factor in selenium status for the prevention of CHD.     

Effect of acute selenium restriction on whole body endogenous selenium and the selenite-exchangeable metabolic pool in the adult rat

The time course of changes in whole body endogenous selenium (Se(end)) was investigated during a short-term (7-day) selenium restriction study in the adult rat. The method of continuous feeding with a stable isotope of selenium was used to permit normal intake of selenium while distinguishing between the dietary and endogenous components of body selenium. Additionally, the effect of short-term selenium restriction on the time course of the selenite-exchangeable metabolic pool (Se-EMP) was investigated. Two groups of adult male rats were intubated with the in vivo stable isotope (74)SeO(3)(2-), then fed a Torula yeast diet (selenium <0.02 microg/g) and either deionized water (-Se group) or deionized water containing selenium as (76)SeO(3)(2-) (0.1 microg selenium/ml) (+Se group). Three animals from each group were killed at 24-hour intervals. Whole body Se(end) and the estimated size of Se-EMP (W(Se-EMP)) were determined using hydride generation-inductively coupled plasma mass spectrometry for isotopic measurements. Whole body Se(end) decreased linearly in the +Se group (Se degrees (end): 54.4 microg; Se(end) at 3 days: 49.3 +/- 2.1; Se(end) at 7 days: 45.2 +/- 2.2). The decrease was exponential for the -Se group (Se degrees (end): 54.4 microg; Se(end) at 3 days: 42.9 +/- 0.3; Se(end) at 7 days: 42.2 +/- 0.7). The value of W(Se-EMP,pl) (microg) was 19.8 +/- 0.6 at 1 day and 19.7 +/- 1.0 at 7 days for the +Se group. The corresponding values for the -Se group were 15.7 +/- 1.5 and 18.8 +/- 0.4. All respective values of W(Se-EMP,pl) for the -Se group were significantly smaller than for the +Se group (P < 0.05), with the exception of values at days 6 and 7. The value of W(Se-EMP,urine) (microg) was 2.1 +/- 0.2 at 1 day, increasing rapidly to 23.5 +/- 1.5 at 7 days for the +Se group. The corresponding values for the -Se group were 3.0 and 23.1.     

Platelet selenium in children with normal and low selenium intake

The concentration of selenium was determined by instrumental neutron activation analysis in erythrocytes, platelets, and plasma of eight dietetically treated children with phenylketonuria (n=6) or maple-syrup-urine disease (n=2) with low selenium intake and for ten children with normal selenium intake. The normal selenium concentration in platelets was about 600 ng/g and about five times higher than in erythrocytes of the same children. A decreased selenium concentration in platelets was seen only when the corresponding concentrations in erythrocytes and plasma were very low. This suggests a special role of selenium in platelets.     

Dietary selenium requirements based on tissue selenium concentration and glutathione peroxidase activities in old female rats

Dietary nutrient requirements for older animals have been studied far less than have requirements for young growing animals. To determine dietary selenium (Se) requirements in old rats, we fed female weanling rats a Se-deficient diet (0.007 μg Se/g) or supplemented rats with graded levels of dietary Se (0–0.3 μg Se/g) as Na₂SeO₃ for 52 weeks. At no point did Se deficiency or level of Se supplementation have a significant effect (P>0.05) on growth. To determine Se requirements, Se response curves were determined for 7 Se-dependent parameters. We found that minimum dietary Se requirements in year-old female rats were at or below 0.05 μg Se/g diet based on liver Se, red blood cell glutathione peroxidase (Gpx1) activity, plasma Gpx3 activity, liver and kidney Gpx1 activity, and liver and kidney Gpx4 activity. In conclusion, this study found that dietary Se requirements in old female rats were decreased at least 50% relative to requirements found in young, rapidly growing female rats. Collectively, this indicates that the homeostatic mechanisms related to retention and maintenance of Se status are still fully functional in old female rats.     

The distribution of selenium and cancer mortality in the continental United States

An hypothesis was proposed that selenium concentration in the environment, as measured by the uptake of this element by forage crops, exerted an apparent effect on cancer incidence, such that cancer mortality in the continental United States was lower where the selenium concentration was high than where the concentration was low. The purpose of the present study is to test this hypothesis for statistical significance and to discover whether the apparent pattern of cancer mortality in relation to selenium distribution holds true with respect to all ages. Two main types of statistical analyses were employed: analysis of variance and trend analysis, both applied to all age groups and both sexes. Data presented in this paper show that significant interactions exist between selenium distribution and sex in relation to deaths caused by cancer of the digestive organs, respiratory organs, and the breast. Geographic variations in selenium may be viewed as variations in the intake of this element in the diet. A significant interaction may thus suggest that the particular cancer in question has in its origin a dietary factor that includes some measure of selenium intake. A discussion involving contributions from various disciplines is presented to explain the significant results reported in this paper. This paper shows that a pattern exists between the geographical distribution of selenium using forage crops as a guide for dietary intake and cancer mortality (ICD 140-209,150-159,160-163, and 174) such that an inverse relationship exists between selenium concentration in an area and cancer mortality in the same area.     

Seminal selenium concentrations and spermatozoal abnormalities in beef bulls

The relationship between seminal selenium (Se) concentration and spermatozoal abnormalities in 24 Angus and 12 Simmental bulls maintained on a Se adequate diet was studied. Two semen samples were collected by electroejaculation 50 days apart from each bull. Measurements of primary and secondary spermatozoal abnormalities, seminal Se concentration, and blood plasma Se concentration were determined at each semen collection. The mean (chi +/- SD ) Se concentration of semen (0.535 +/- 0.267) was approximately 8 fold greater than the Se concentration of blood plasma (0.069 +/- 0.066) and the values were similar for both collections. Spermatozoa concentration was correlated (r = 0.50; P<.01) with seminal Se concentration; however, seminal Se concentration was not highly correlated (P<.01) with primary spermatozoal abnormalities (r = -0.29) and secondary spermatozoal abnormalities (r = 0.16). This study indicates that the Se concentration of semen is high relative to blood plasma in bulls maintained on a Se adequate diet; however, the seminal Se concentration is not highly correlated with spermatozoal abnormalities.     

Determination of selenium in serum by FI-HG-AAS and calculation of dietary intake

A method was developed for the determination of selenium concentration in serum by flow injection-hydride generation-atomic absorption spectrometry (FI-HG-AAS) following microwave digestion of serum samples and reduction of selenate to selenite. The detection limit of the method was 0.3 μg Se/L and the characteristic concentration, corresponding to the 0.0044 absorbance signal, was 0.12 μg Se/L. The results from the analysis of two Seronorm standard reference materials showed good agreement with the certified values. The method was then used to analyze selenium in sera of Austrian and Slovenian people for the calculation of dietary intakes. The selenium concentrations in sera of mothers at delivery, their neonates, and the male and female adults were 71 ± 14, 42 ± 6, 75 ± 21, and 65 ± 16 μg/L for the Austrians and 62 ± 15, 34 ± 7, 70 ± 12, and 66 ± 15 μg/L for the Slovenians. The dietary intakes of selenium of the mothers and the male and the female adults were calculated as 52, 37, and 46 μg/d for the Austrians and 45, 38, and 32 μg/d for the Slovenians.     

Effect of dietary selenium on the promotion of hepatocarcinogenesis by 3,3', 4,4'-tetrachlorobiphenyl and 2,2', 4,4', 5,5'-hexachlorobiphenyl

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that have promoting activity in the liver. PCBs induce oxidative stress, which may influence carcinogenesis. Epidemiological studies strongly suggest an inverse relationship between dietary selenium (Se) and cancer. Despite evidence linking Se deficiency to hepatocellular carcinoma and liver necrosis, the underlying mechanisms for Se cancer protection in the liver remain to be determined. We examined the effect of dietary Se on the tumor promoting activities of two PCBs congeners, 3,3', 4,4'-tetrachlorobiphenyl (PCB-77) and 2,2', 4,4', 5,5'-hexachlorobiphenyl (PCB-153) using a 2-stage carcinogenesis model. An AIN-93 torula yeast-based purified diet containing 0.02 (deficient), 0.2 (adequate), or 2.0 mg (supplemental) selenium/kg diet was fed to Sprague-Dawley female rats starting ten days after administering a single dose of diethylnitrosamine (150 mg/kg). After being fed the selenium diets for 3 weeks, rats received four i.p. injections of either PCB-77 or PCB-153 (150 micromol/kg) administered every 14 days. The number of placental glutathione S-transferase (PGST)-positive foci per cm(3) and per liver among the PCB-77-treated rats was increased as the Se dietary level increased. Unlike PCB-77, rats receiving PCB-153 did not show the same Se dose-response effect; nevertheless, Se supplementation did not confer protection against foci development. However, the 2.0 ppm Se diet reduced the mean focal volume, indicating a possible protective effect by inhibiting progression of preneoplastic lesions into larger foci. Cell proliferation was not inhibited by Se in the liver of the PCB-treated groups. Se did not prevent the PCB-77-induced decrease of hepatic Se and associated reduction in glutathione peroxidase (GPx) activity. In contrast, thioredoxin reductase (TrxR) activity was not affected by the PCBs treatment or by Se supplementation. These findings indicate that Se does not inhibit the number of PGST-positive foci induced during promotion by PCBs, but that the size of the lesions may be inhibited. The effects of Se on altered hepatic foci do not correlate with its effects on GPx and TrxR.