Biomedical subjects

R W Scholz

Publications and source records attributed to R W Scholz.

At least 19 recordsLinked to original sources

PubMed2004

The HOCS paradigm shift from disciplinary knowledge (LOCS)--to interdisciplinary evaluative, system thinking (HOCS): what should it take in science-technology-environment-society oriented courses, curricula and assessment?

Given the current world state of affairs, striving for sustainability and the consequent paradigm shift: growth-to-sustainable development, correction-to-prevention and options selection-to-options generation: the corresponding paradigm shift in science-technology-environment-society (STES) education is unavoidable. Accordingly, the essence of the current reform in STES education, worldwide, is a purposed effort to develop students' higher-order cognitive skills (HOCS) capability; i.e., question-asking, critical system thinking, decision making and problem solving, at the expense of the "delivery" of lower-order cognitive skills (LOCS)-oriented knowledge. This means a paradigm shift from the contemporary prevalent LOCS algorithmic teaching to HOCS evaluative learning and HOCS-promoting courses, curricula, teaching strategies and assessment methodologies, leading, hopefully to evaluative thinking and transfer. Following the formulation of selected relevant axioms, major paradigm shift in STES research and education for sustainability have been identified. The consequent shift, in the STES context, from disciplinary to inter- and transdisciplinary learning, in science technology and environmental engineering education is discussed, followed by selected examples of successfully implemented HOCS-promoting courses, and assessment methodologies. It is argued, that transferable "HOCS learning" for sustainability can and should be done.

Clinical Competence↗

PubMed2001

Microsomal glutathione S-transferase A1-1 with glutathione peroxidase activity from sheep liver: molecular cloning, expression and characterization.

A 25 kDa subunit of glutathione S-transferase (GST) from sheep liver microsomes (microsomal GSTA1-1) with a significant selenium-independent glutathione peroxidase activity has been isolated and characterized. Several analytical criteria, including EDTA stripping, protease protection assay and extraction with alkaline Na(2)CO(3), indicate that the microsomal GSTA1-1 is associated with the inner microsomal membrane. The specific cDNA nucleotide sequence reveals that the enzyme is made up of 222 amino acid residues and shares approx. 73-83% sequence similarity to Alpha-class GSTs from different species. The molecular mass, as determined by electrospray mass ionization, is 25611.3 Da. The enzyme is distinct from the previously reported rat liver microsomal GST in both amino acid sequence and catalytic properties [Morgenstern, Guthenberg and DePierre (1982) Eur. J. Biochem. 128, 243-248]. The microsomal GSTA1-1 differs from the sheep liver cytosolic GSTs, reported previously from this laboratory, in its substrate specificity profile and molecular mass [Reddy, Burgess, Gong, Massaro and Tu (1983) Arch. Biochem. Biophys. 224, 87-101]. In addition to catalysing the conjugation of 4-hydroxynonenal with GSH, the enzyme also exhibits significant glutathione peroxidase activity towards physiologically relevant fatty acid hydroperoxides, such as linoleic and arachidonic acid hydroperoxides, as well as phosphatidylcholine hydroperoxide, but not with H(2)O(2). Thus the microsomal GSTA1-1 isoenzyme might have an important role in the protection of biological membranes against oxidative damage.

Amino Acid Sequence↗

PubMed2001

Risk perception of heavy metal soil contamination and attitudes toward decontamination strategies.

Contaminated soils are a common environmental risk all over the world. One major source of risk is heavy metal soil contamination caused by industrial emissions. This quasiexperimental study investigated the perception of these risks by exposed and nonexposed people, their attitudes toward bioremediation methods using hyperaccumulating plants, and the influence of long-term aspects of sustainability on the acceptance of bioremediation methods. Major findings were that people living in a contaminated area perceived the risk of the heavy metal soil contamination as higher than the general risk of contamination. Second, a factor analysis showed that the factors dread, control, and catastrophic potential were relevant for the perception and valuation of low-dose environmental risks such as the contamination of the investigated area. In addition, a cluster analysis showed that the risk of heavy metal soil contamination was perceived as similar to that of oil contamination, ozone layer, preservatives and genetic technology. It was perceived indifferently with regard to dread. The uncontrollability of heavy metal soil contamination was estimated as medium, and its catastrophic potential as low. Third, exposed and nonexposed participants preferred bioremediation methods to classical methods (e.g., excavation and chemical treatment of the soil), because they perceived the environmental and esthetical performance of the bioremediation as important criteria. Sustainability or precautionary issues, such as the prevention of harm for future generations, were highly correlated with the acceptance of the use of bioremediation methods in people's residential areas.

Adult↗

PubMed1997

Glutathione-dependent factors and inhibition of rat liver microsomal lipid peroxidation.

The effects of reduced glutathione (GSH) and glutathione disulfide (GSSG) on lipid peroxidation were investigated in rat liver microsomes containing deficient or adequate amounts of alpha-tocopherol (alpha-TH). Rates of formation of thiobarbituric acid reactive substances (TBARS) as well as rates of consumption of alpha-TH and O2 were decreased by GSH and were more pronounced in the NADPH-dependent assay system than in the ascorbate-dependent system. The GSH-dependent inhibition of lipid peroxidation was potentiated by GSSG in the NADPH-dependent assay system, but it had no effect in the nonenzymatic system. Diphenyliodonium chloride, an inhibitor of NADPH cytochrome P-450 reductase, completely prevented lipid peroxidation in the NADPH-dependent assay system whereas it had no effect on the ascorbate-dependent system. This is further evidenced by the fact that purified rat liver microsomal NADPH cytochrome P-450 reductase (EC 1.6.2.4) was inhibited approximately 24% and 52% by 5 mM GSH and 5 mM GSH + 2.5 mM GSSG, respectively. Glutathione disulfide alone had no effect on reductase activity. Similarly, other disulfides such as cystine, cystamine and lipoic acid were without effect on reductase activity. These results clearly delineate different mechanisms underlying the combined effects of GSH and GSSG on microsomal lipid peroxidation in rat liver. One mechanism involves recycling of microsomal alpha-TH by GSH during oxidative stress via a labile protein, ostensibly associated with "free radical reductase" activity. A second glutathione-dependent mechanism appears to be mediated through the inhibition of NADPH cytochrome P-450 reductase. The enhanced inhibition by GSH + GSSG of microsomal lipid peroxidation in the NADPH-dependent assay system suggests suppression of the initiation phase at the level of NADPH cytochrome P-450 reductase which is independent of microsomal alpha-TH.

Animals↗

PubMed1997

Effects of vitamin E and selenium on antioxidant defense in rat heart.

Heart mitochondria, isolated from rats fed diets deficient or supplemented with vitamin E (E) and/or selenium (Se), were subjected to time-course assays of lipid peroxidation stimulated by ascorbate/ADP/Fe3+. Mitochondria depleted of alpha-tocopherol (alpha-TH) peroxided rapidly as assessed by formation of thiobarbituric acid reactive substances (TBARS). Formation of TBARS was strongly inhibited in mitochondria from rats fed diets supplemented with E. Selenium deficiency, reduced glutathione (GSH), glutathione disulfide (GSSG) or GSH + GSSG did not affect the course of lipid peroxidation in mitochondria from rats supplemented or deficient in E. Combined E and Se deficiency resulted in significantly lower total (oxidized+reduced) mitochondrial coenzyme Q-9 (CoQ-9) concentration compared with control rats supplemented with dietary E and Se. Time-course changes in mitochondrial alpha-TH and total CoQ-9 during oxidizing conditions were minor in +E rats. Total CoQ-9 was reduced substantially, however, during the course of lipid peroxidation in mitochondria depleted of alpha-TH. Selenium-dependent glutathione peroxidase (Se-GSHPx) activity was reduced by approximately 96% in heart cytosol, and to a somewhat lesser extent in mitochondria, by dietary Se deficiency. Non-Se GSHPx activity was not detected in heart cytosol but was detected in very small amounts in heart mitochondria. Glutathione S-transferase activity of heart cytosol was decreased in E and/or Se deficiency. The results of these experiments indicate that membrane alpha-TH was most effective in inhibiting lipid peroxidation in heart mitochondria.

Animals↗

PubMed1996

Inhibition of rat liver microsomal NADPH cytochrome P450 reductase by glutathione and glutathione disulfide.

Previously we have demonstrated inhibition of lipid peroxidation by reduced glutathione (GSH) in rat liver microsomes that is dependent upon the presence of alpha-tocopheral (alpha-TH) in the membranes. Glutathione disulfide (GSSG) potentiated the inhibitory effect of GSH in an enzymatic (NADPH-dependent) lipid peroxidation system in rat liver microsomes; however, inhibition by GSH + GSSG is independent of alpha-TH. When we repeated these experiments with a non-enzymatic system (ascorbate/ADP) to stimulate lipid peroxidation, GSSG did not potentiate the inhibitory effect of GSH. To delineate the mechanism of inhibition of microsomal lipid peroxidation by GSH + GSSG, we examined the effects of these compounds on cytochrome P-450 reductase (EC 1.6.2.4), an important component of the NADPH-dependent enzymatic lipid peroxidation system. It was observed that GSH alone caused about 25% and 21% inhibition of reductase activity in crude microsomes and partially purified enzyme preparations, respectively. There was no inhibition of reductase activity by GSSG alone in either crude microsomes or partially purified enzyme preparations. However, when added together, GSH and GSSG enhanced the inhibition of reductase activity in crude microsomes and partially purified enzyme by 39% and 56%, respectively. We speculate that one possible mechanism for the inhibition of NADPH-dependent lipid peroxidation by GSH + GSSG is, in part, due to inhibition of NADPH cytochrome P-450 reductase, thus affecting the initiation phase of lipid peroxidation.

Animals↗

PubMed1996

Glutathione-dependent protection against lipid peroxidation in sheep liver microsomes.

In the present studies we have described a glutathione-dependent system in sheep liver microsomes that protects against membrane lipid peroxidation initiated by either Fe+2/NADPH or Fe+2/ascorbate. Glutathione protected against lipid peroxidation in microsomes containing a wide range of alpha-tocopherol levels (0.02-0.11 microgram/mg protein). The addition of glutathione disulfide alone had no effect on microsomal lipid peroxidation, however, it prolonged the protection afforded by glutathione, particularly in assays containing Fe+2/NADPH. Whereas the glutathione-dependent protection was very labile, with loss of activity demonstrated in microsomes stored at 4 degrees C for 24 hours, the combined effect of glutathione and glutathione disulfide was not affected by storage. The glutathione S-transferase inhibitors, bromosulphothalein and S-hexylglutathione, reversed the protection observed with glutathione, indicating a possible role for microsomal glutathione S-transferases in this protection, but not that observed by the combination of glutathione and glutathione disulfide. In general, our findings support previous results observed with rat liver microsomes and suggest that microsomal glutathione S-transferases may be involved in the glutathione-dependent protection in sheep liver microsomes.

Animals↗

PubMed1996

Effects of maternal vitamin E and selenium status during the perinatal period on age-related changes in tissue concentration of vitamin E in rat pups.

Long-Evans hooded female rats previously acclimated to one of four experimental diets differing in their vitamin E (E) and selenium (Se) contents were used in these studies. The basal diet (-E -Se) was marginal in E (15 IU/kg) and Se (0.03 mg/kg) content. Three additional diets, -E, +Se, +E-Se and +E +Se were prepared by supplementing the basal diet with dl-alpha-tocopheryl acetate to contain 150 IU/kg or with sodium selenite to contain 0.5 mg/kg, as required. The rats were mated and the pups born were used to provide plasma, heart, lung and liver tissue for E analyses at postpartum intervals from birth (prior to nursing) to 21 days of age. Differences in Se nutrition of the dams during the perinatal period did not affect the E content of tissues of the rat pups. There were no significant differences (P > 0.05) in E content of plasma or liver tissue at birth in rat pups regardless of the maternal E status. Heart and lung tissue, however, were significantly higher (P < 0.05) in E concentration at birth in pups whose dams were fed the +E diets. Rat pups nursing -E dams had consistently low E content in each of the tissues throughout the postpartum period which did not differ from levels determined prior to nursing. Pups nursing +E dams had elevated E concentration in each of the tissues during the postpartum period. Liver tissue provided the most remarkable response in that E concentration increased approximately 30-fold within 4 days postpartum and then decreased abruptly. The results of these studies suggest a differential transfer of E to rat tissues during gestation. Net placental transfer of E to fetal liver appeared to be very low and was not influenced by marked differences in maternal dietary E. In contrast, preferential incorporation into heart and lung tissue during gestation was shown by the data. In all tissues, increased E content following birth was attributed to ingestion of colostrum and milk containing elevated amounts of the vitamin.

Aging↗

PubMed1996

Effects of maternal vitamin E and selenium status during the perinatal period on age-related changes in heart, lung and liver microsomal lipid peroxidation in rat pups.

Female Long-Evans rats of breeding age were acclimated to one of four experimental diets differing in their vitamin E (E) and selenium (Se) contents. These animals were bred and the offspring produced were nursed by their respective dams from birth through 21 days postpartum. Rat pups were killed at postpartum intervals of 4, 9, 14 and 21 days and heart, lung and liver tissue used for isolation of microsomes. Microsomes were used for quantitation of E content as well as for assays of lipid peroxidation (thiobarbituric acid reactive products formation) using an ascorbate/ADP nonenzymatic assay system. Microsomal E content was lower in heart and lung tissues of rat pups at each postpartum interval compared with maternal levels. Liver microsomal E was higher in rat pups at day 4 postpartum compared with maternal levels. Significant differences (P < 0.05) in microsomal E content of rat pup tissues were associated with maternal vitamin E status during the perinatal period and not to differences in dietary Se. In vitro lipid peroxidation was highest in rat pups nursing dams of low E status, the magnitude of which was greatest in heart and liver microsomes. Lung microsomes, in contrast, peroxidized at very low rates compared with heart and liver microsomes. These effects were independent of maternal Se status. Microsomal lipid peroxidation in tissues of rat pups was lowest at the earliest postpartum interval studied (4 days) and, in general, increased with postpartum age. Reduced glutathione did not inhibit lipid peroxidation in heart or lung microsomes but was effective in this respect in liver microsomes of rat pups as early as 4 days postpartum.

Aging↗

PubMed1994

Dietary vitamin E and selenium effects on resistance to oxidative stress in rat liver mitochondria.

Mitochondria-rich fractions isolated from livers of rats fed diets differing in their vitamin E (E) and/or selenium (Se) contents were subjected to NADPH/ADP/Fe(3+)- dependent assays of lipid peroxidation. Addition of GSH resulted in an inhibition, or lag period, of lipid peroxidation in mitochondria from rats supplemented with E. This effect was independent of the Se status of the rats. Addition of GSH + GSSG did not potentiate the lag period over that observed with GSH alone. Significant changes in mitochondrial alpha-TH during lipid peroxidation, either in the presence or absence of GSH, were not observed. Total protein thiol (PrSH) content of native mitochondria was lower in rats fed a diet deficient in both E and Se, compared to the other dietary groups. Addition of GSH or GSH + GSSG maintained mitochondrial PrSH at higher levels during lipid peroxidation than in control assays without added GSH/GSSG. Addition of GSSG alone decreased PrSH in mitochondria prepared from all rats regardless of their E or Se status. Reduced ubiquinone-9 (U-9) and the % of total U-9 and U-10 in the reduced form were significantly decreased in liver tissue from rats fed the diet deficient in both E and Se.

Animals↗

PubMed1993

Increased thromboxane A2 synthesis by rat lung neutrophils during selenium deficiency.

Modulation of cellular hydroperoxide levels is considered one of the important physiological mechanisms for regulating the synthesis of prostaglandins (PGs) and leukotrienes (LTs) in mammalian cells. Both vitamin E and selenium (Se) have the potential to affect the concentration of peroxides and, thus, the biosynthesis of eicosanoids. To gain insight into some of the molecular mechanisms underlying the regulation of the arachidonic acid cascade by vitamin E and Se, we have investigated the influence of altered vitamin E and Se nutrition on the ability of polymorphonuclear leukocytes (PMNs) derived from endotoxin-challenged lung to secrete arachidonic acid metabolites. Selenium deficiency had no significant effect (p > 0.05) on lavage fluid levels of thromboxane (TX) B2, LTB4 or LTC4. Vitamin E deficiency, however, led to a significant increase in LTB4 recovered from lavage fluid while having no effect on TXB2. In contrast, Se deficiency, although producing no discernible effects on the production of LTB4, resulted in a significant increase in the release of TXB2 by PMNs. An increase in TXB2 release was seen in both in vitro-stimulated and nonstimulated PMNs. Vitamin E deficiency appeared to induce an enhancement of LTB4 release by PMNs but the increase was not statistically significant. No detectable levels of LTC4 were found in PMN cultures stimulated with either zymosan or A23187. Thus, these studies indicate that deficiencies of either Se or vitamin E lead to alterations in the metabolism of arachidonic acid in the lung.

Animals↗

PubMed1992

Selenium deficiency alters the lipoxygenase pathway and mitogenic response in bovine lymphocytes.

We investigated the effect of altered selenium (Se) nutrition on arachidonic acid oxidation in immune cells. Experiments were conducted with peripheral blood lymphocytes obtained from dairy cattle fed diets either supplemented with or deficient in Se. The results indicate that the concanavalin A-stimulated lymphocyte proliferation was significantly lower in Se-deficient cows. When stimulated by calcium ionophore A23187, the lymphocytes derived from Se-deficient cows produced significantly less 5-hydroxyeicosatetraenoic acid (5-HETE) and leukotriene B4 (LTB4) than those obtained from Se-supplemented cows. When included in cell cultures from animals fed +Se diets, 5-HETE and LTB4 elicited a partial reversal of the inhibition of lymphocyte proliferation by either hydrocortisone or nordihydroguaiaretic acid. Based on this information, we postulate that dietary Se status, which in turn determines tissue Se concentration, plays an important role in the regulation of arachidonate metabolism by way of the 5-lipoxygenase pathway. This may be one of the biochemical mechanisms underlying the inhibition of lymphocyte proliferation and the decrease in resistance to infectious diseases observed in Se-deficient animals.

Animals↗

PubMed1991

Increased 12-HETE production in bovine lymphocytes during selenium deficiency.

When peripheral blood lymphocytes were incubated with arachidonic acid in the presence of Ca++ ionophore (A23187), the cells from the selenium-deficient dairy cows produced significantly greater quantities of 12-hydroxyeicosatetraenoic acid (12-HETE) than the cells from the selenium-supplemented animals. The major product of reaction was verified as 12-HETE by cochromatography with a 12-HETE standard on an HPLC and structural analysis by GC-MS. Additionally, concanavalin A-stimulated lymphocyte proliferation was significantly decreased in cells from the Se-deficient cows. Furthermore, 12-HETE generated by the A23187-stimulated lymphocytes inhibited lymphocyte proliferation when added to Se-supplemented cell cultures. These observations suggest that self-regulation of lymphocyte proliferation might be mediated by 12-HETE production, especially during an altered nutritional state such as Se deficiency.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1991

Dietary selenium effects on milk eicosanoid concentration in dairy cows during coliform mastitis.

The effect of selenium deficiency on the product profile of arachidonic acid oxidation by enzymatic pathways in Holstein cows with experimentally-induced coliform mastitis was investigated. The animals were fed dairy rations containing 0.05 mg Se/kg dry matter, with the supplemented group receiving additional Se to increase the dietary concentration to approximately 0.35 mg Se/kg dry matter. Cows were inoculated intracisternally with 30 colony-forming-units of Escherichia coli at 14-16 weeks of lactation. Eicosanoids and bacteria numbers were recorded at various intervals of time for 60 h postinoculation. Milk from cows fed the Se-depleted diet had significantly higher (p less than 0.05) concentrations of TXB2 between 24 and 48 h and 6-keto-PGF1 alpha between 24 and 60 h postinoculation. Milk PGE2 concentration was significantly higher in the Se-deficient group at 24 h, whereas LTB4 was higher between 36 and 60 h postinoculation in the Se-deficient cows (p less than 0.05). Milk bacteria numbers were significantly higher between 16 and 24 h postinoculation in the Se-deficient group and three of the four cows in this group required euthanasia, whereas all four cows in the Se-supplemented group recovered without therapeutic intervention. These data indicate marked effects of dietary Se on milk eicosanoid concentrations in response to an E. coli infection. The changes in eicosanoid concentrations may be associated with the altered pathogenesis and outcome of mastitis in a Se-deficient state.

6-Ketoprostaglandin F1 alpha↗

PubMed1990

The induction of specific rat liver glutathione S-transferase subunits under inadequate selenium nutrition causes an increase in prostaglandin F2 alpha formation.

We have reported previously that a dietary deficiency in selenium results in an increase in glutathione S-transferase (GST) activity of various rat tissues. In order to verify that the increased GST activity observed in a selenium deficiency results from increased synthesis of GST protein, cytosolic fractions of livers obtained from rats fed selenium-deficient and selenium-supplemented diets were analyzed by Western (protein) blots. Antisera raised against purified individual GST subunits (Ya, Yb, and Yc) were used to detect the corresponding subunits on the blots. The Ya subunit was induced 2.5-fold in the selenium-deficient state. The amount of Yc subunit also increased significantly (p less than 0.05) in selenium deficiency but not to the extent of the Ya subunit. The Yb subunit was not significantly affected by altered selenium nutritional status. A corresponding increase in poly(A) RNAs coding for the Ya and Yc subunits was also observed by Northern blot analysis. Transcriptional activity of GST YaYc genes was elevated by approximately 2-fold in purified nuclei isolated from selenium-deficient rat livers, which is sufficient to account for the increase in YaYc mRNA levels. Therefore, it appears that transcriptional activation of rat liver YaYc genes is the primary cause for the elevation of the corresponding gene products in the selenium-deficient state. Since the GSTs, especially the isozymes containing Ya subunit, have been implicated in the formation of prostaglandin (PG) F2 alpha, we investigated the effect of selenium deficiency on the PGF2 alpha-forming activity using a specific inhibitor of GSTs, S-decyl-GSH. In rats fed a nutritionally adequate diet, the activity inhibited by S-decyl-GSH accounted for at least half of the conversion of PGH2 to PGF2 alpha. During selenium deficiency, this GST-catalyzed activity was approximately doubled with no change in PGF2 alpha formation by other pathways, resulting in a 2-fold increase in overall synthesis of PGF2 alpha. These data strongly support a role of GSTs, especially those composed of the Ya size subunit, in the synthesis of PGF2 alpha from PGH2.

Animals↗

PubMed1990

Glutathione disulfide enhances the reduced glutathione inhibition of lipid peroxidation in rat liver microsomes.

Experiments were undertaken to examine the effects of reduced (GSH) and oxidized (GSSG) glutathione on lipid peroxidation of rat liver microsomes. Dependence on microsomal alpha-tocopherol was shown for the GSH inhibition of lipid peroxidation. However, when GSH (5 mM) and GSSG (2.5 mM) were combined in the assay system, inhibition of lipid peroxidation was enhanced markedly over that with GSH alone in microsomes containing alpha-tocopherol. Surprisingly, the synergistic inhibitory effect of GSH and GSSG was also observed for microsomes that were deficient in alpha-tocopherol. These data suggest that there may be more than one factor responsible for the glutathione-dependent inhibition of lipid peroxidation. The first is dependent upon microsomal alpha-tocopherol and likely requires GSH for alpha-tocopherol regeneration from the alpha-tocopheroxyl radical during lipid peroxidation. The second factor appears to be independent of alpha-tocopherol and may involve the reduction of lipid hydroperoxides to their corresponding alcohols. One, or possibly both, of these factors may be activated by GSSG through thiol/disulfide exchange with a protein sulfhydryl moiety.

Animals↗

PubMed1990

Elevation of rat liver mRNA for selenium-dependent glutathione peroxidase by selenium deficiency.

Selenium-dependent glutathione peroxidase (Se-GSH-Px, GSH-H2O2 oxidoreductase EC 1.11.1.9) is the best characterized selenoprotein in higher animals, but the mechanism whereby selenium becomes incorporated into the enzyme protein remains under investigation. To elucidate the mechanism of insertion of selenium into Ge-GSH-Px further, we have systematically analyzed and compared the results of Western blot, in vitro translation immunoprecipitation, and Northern blot experiments conducted with liver proteins and RNAs obtained from rats fed on selenium-deficient and selenium-supplemented diets. The anti-serum employed in this study was raised against an electrophoretically pure Se-GSH-Px preparation obtained from rat livers by a simplified purification procedure involving separation by high performance liquid chromatography on a hydrophobic interaction column. Different forms of Se-GSH-Px, including apo-protein, cross-reacted with this antiserum and Western blot analysis found no Se-GSH-Px protein present in livers from rats fed on selenium-deficient diets. By contrast, a distinct protein band corresponding to purified Se-GSH-Px was detected in livers from selenium-supplemented animals, a result consistent with the finding that the Se-GSH-Px activity was reduced to undetectable levels in livers of selenium-deficient rats. The in vitro translation experiments, however, indicated not only that mRNA for Se-GSH-Px was present during selenium deficiency but also that its translation products contained 2-3-fold as much immunoprecipitable protein as the products of poly(A) RNA from livers of selenium-supplemented rats. This result suggests that the Se-GSH-Px mRNA may be increased in the selenium-deficient state. Elevated levels of Se-GSH-Px mRNA were directly demonstrated in Northern blot experiments employing cDNA clone pGPX1211 as a probe. A similar increase in Se-GSH-Px mRNA was observed in such other tissues as kidney, testis, brain, and lung tissue, in selenium-deficient states. The present data support the co-translational mechanism for the incorporation of selenium into Se-GSH-Px in rat liver.

Animals↗

PubMed1990

[Assessment of health risk due to cadmium contaminated house gardens].

An epidemiological survey was conducted on the cadmium intoxication of 132 residents living on former sewage fields. Besides 'global biological monitoring', the relation between the cadmium secretion in urine and the load of cadmium of the kitchen gardens and flower gardens was analysed. There were significant correlations between the cadmium concentration of the residents' garden soil and their daily urine secretion, particularly for older nonsmokers who admitted "at least occasional consumption" of products from their gardens. The value of applying non-parametric correlation coefficients is proven.

Adolescent↗