[Studies on enzymatic glycerolysis of palm oil by lowering temperature proceedingly in solid state].

Enzymatic glycerolysis of palm oil was studied in solid state with a lipase from Pseudomonus fluorescens as catalyst. The influences of molar ratio of glycerol to oil, reaction temperatures and temperature control on the accumulation of monoglyceriods in reaction mixtures were investigated. The suitable initial reaction temperature should be the minimum co-melting point of reactants. The monoglycerides contents in equilibrium state were approximately 30% at 48 degrees C or higher. An increment of 13% of monoglycerides content was obtained under the optimum temperature programming comparing with the normal equilibrium state.

Selenium supplementation of Chinese women with habitually low selenium intake increases plasma selenium, plasma glutathione peroxidase activity, and milk selenium, but not milk glutathione peroxidase activity.

Twenty-one pregnant women living in Xichang County, China, a selenium-deficient area, were divided into two groups and given either a placebo (n = 10) as yeast or selenium-enriched yeast tablets (n = 11) to provide 100 microg selenium per day. This supplementation was begun the last trimester of pregnancy and continued for 3 months after parturition. Plasma selenium levels and glutathione peroxidase (GPX) activity steadily declined in supplemented women, but a curvilinear response occurred in milk selenium and GPX activity in both supplemented and deficient women and in plasma selenium and GPX activity in deficient women. The milk selenium levels were higher in supplemented women but there were no differences in the milk GPX activity between the two groups of women. The plasma alpha-tocopherol concentrations declined after parturition in both groups but no differences were found between the two groups of women. Plasma thiobarbituric acid reactive substances declined in supplemented women but showed a curvilinear response in unsupplemented women, suggesting peroxidative stress in these women. GPX, selenium, and peroxidative responses in plasma and milk following parturition is advocated as a new method to assess selenium status of lactating women.

Distribution of selenium between plasma fractions in guinea pigs and humans with various intakes of dietary selenium.

The distribution of selenium between the plasma fractions was investigated in guinea pigs fed various levels (basal, 0.5, 1.0, 2.0, 4.0, 6.0 and 8.0 mg Se/kg) of dietary selenomethionine (Semet) and in humans living in different areas of China with different selenium status. There was a corresponding increase of selenium concentration in liver, kidney, brain, testis, spleen, heart and muscle with each increase of dietary selenium, but there were no increases of glutathione peroxidase (GPX) activity in liver, brain, testis, heart or muscle in pigs fed any of the selenium levels as compared to controls fed a basal commercial diet. On a percentage distribution basis, the selenium in selenoprotein P decreased and that in the albumin fraction increased with increased dietary intakes of selenium as Semet. The ratios of selenium to albumin in either the plasma or the albumin fractions increased with each increase in dietary selenium. The greatest percentage of selenium was in the albumin fraction of Chinese living in the high selenium areas whereas the greatest amount was in the selenoprotein P fraction in subjects living in deficient and adequate areas of China. Increases in the ratios of selenium to albumin in either the plasma or the albumin fraction also occurred with increases of selenium intake of these subjects. The results indicate that the distribution of selenium in plasma fractions reflect the levels of dietary intakes of Semet.

[Progress in the study of mammalian selenoprotein].

Selenium is an essential trace element for animals and humans. Selenium exerts its biological function largely through selenoproteins. Up to now nine selenoproteins' cDNAs have been cloned and sequenced, which are cellular glutathione peroxidase (cGPX), extracellular glutathine peroxidase(eGPX), phospholipid hydroperoxidase glutathione peroxidase(PHGPX), gastrointestinal glutathione peroxidase (GPX-GI), type I iodothyronine 5'-deiodinase (ID I), type 2 iodothyronine 5'-deiodinase(ID II), type III iodothyronine 5-deiodinase(ID III), selenoprotein P (Se-P) and selenoprotein W. In all these selenoproteins Se is incorporated into the protein molecule via the selenocysteinyl-tRNA which recognizes the specific UGA codons in mRNA to insert selenocysteine into the primary structure of selenoproteins.

Changes in myocardial thyroid hormone metabolism and alpha-glycerophosphate dehydrogenase activity in rats deficient in iodine and selenium.

Weanling Wistar rats were fed on diets prepared from grain from areas deficient in I and Se where Keshan disease in endemic. Rats were divided into four groups, each of twelve rats, and received a diet supplemented with: I, Se, I + Se or nothing. At 8 weeks after weaning, myocardial alpha-glycerophosphate dehydrogenase (EC 1.1.1.8; alpha-GPD) activity and indices of Se and thyroid hormone status were determined. The group supplemented with iodine had increased plasma thyroxine levels. There was no difference in plasma triiodothyronine concentration between the groups but triiodothyronine levels in heart were reduced in the Se-supplemented group. Se supplementation increased myocardial glutathione peroxidase activity (EC 1.11.1.9) and the type I 5'-deiodinase (EC 3.8.1.4) activity in rat liver, but no type I 5'-deiodinase activity was detected in heart. alpha-GDP activity in heart was increased in group supplemented with Se, I or both. There was a significant relationship (P < 0.05) between myocardial alpha-GDP activity and plasma thyroxine levels but not between alpha-GDP and myocardial glutathione peroxidase activity. The results indicate that iodine may be more important than Se in energy metabolism in the myocardium, which may give a new insight for the study of the aetiology of Keshan disease in areas where foodstuffs are deficient in both Se and I.

[Method of cyanogen bromide-fluorimetry determination of trace amount of selenomethionine in grain and blood].

Selenomethionine (SeMet) reacted with cyanogen bromide (BrCN) quantitatively forms CH3SeCN. After extracted with CHCl3, the Se of CH3SeCN is acid-digested to Se(IV). Then 2,3-diaminonaphthalene is used to determine the fluorescent Se value of 4,5-benzopiaselenol. The determination limit of this method was 3 ng/g SeMet. The accuracy of 10-500 ng Se in SeMet standard was 91.8%-97.6%. RSD was 1.9%-6.3%. Recoveries for grain and blood were 92.3%-96.7%. RSD was 2.7%-5.1%. The RSD for samples was 2.7%-9.0%. Selenocystine, selenocystiene selenite and methionine did not interfere with the determination.

Studies on human dietary requirements and safe range of dietary intakes of selenium in China and their application in the prevention of related endemic diseases.

The human dietary selenium requirement in China has been estimated by various methods. The minimum dietary selenium requirement for the prevention of Keshan disease (KD) was found to be around 17 micrograms/d. On the other hand, an intake of 40 micrograms/d is required to maintain the plasma glutathione peroxidase (GPx) activity at plateau. Hence 40 micrograms/d is considered as the adequate dietary selenium requirement. Studies conducted in a chronic selenosis area indicate that the toxic dietary selenium intake (adverse effect level), which would maintain the characteristic fingernail changes, was approximately 1600 micrograms/d. The mean value of dietary selenium intakes, which enabled the five patients to recover from fingernail lesions, was found to be 819 +/- 126 micrograms/d. At a 95% confidence limit, the lower limit is around 600 micrograms/d. Therefore, 600 and 400 micrograms/d were suggested as the individual daily maximum safe selenium intake and the safe dietary selenium intake, respectively. The results were used in the prevention of Se-related endemic KD and Kashin-Beck disease (KBD).

[Selenium deficiency and thyroid hormone metabolism and function].

Type I 5'-deiodinase is a Se-containing enzyme. If Se is deficient, the deiodinase activity would be inhibited, the level of circulation T4 will be elevated, and the concentration T3 in peripheral tissues will be decreased. Se deficiency will also accelerate the iodine depletion of thyroid and may even exacerbate some detrimental effects of iodine deficiency. Possibly Se deficiency is involved in the occurrence and development of iodine deficient disorders. Keshan disease, with Se deficiency as the major cause, was also observed a change of thyroid hormone metabolism. The change of respiratory enzyme activities in myocardium of Keshan disease is in the way somewhat like that of hypothyroidism caused by iodine deficiency. The metabolic change of thyroid hormone after Se deficiency or iodine deficiency may be related to the occurrence of Keshan disease.

Biochemical studies of a selenium-deficient population in China: measurement of selenium, glutathione peroxidase and other oxidant defense indices in blood.

Selenium deficiency is necessary for the development of the cardiomyopathy known as Keshan disease. Healthy boys and men (19-22 per group) from a low selenium area (Dechang County) and from an area where sodium selenite was added to salt (Mianning County) were studied. Keshan disease was endemic in Dechang but occurred rarely in Mianning. After an initial blood sampling, each subject received daily selenium supplements (100 micrograms selenium for boys and 200 micrograms for men) as sodium selenate for 14 d. Blood was sampled again at 7 and 14 d. Boys from Dechang had blood selenium levels similar to levels reported for patients with Keshan disease. Plasma glutathione peroxidase activity in boys and men from Dechang was 33 and 43%, respectively, of values from the corresponding groups in Mianning. Comparison of plasma selenium concentrations in boys and men from Dechang gave values of 33 and 38%, respectively, of the corresponding groups in Mianning. Selenium status did not affect red blood cell superoxide dismutase or catalase activities. Plasma vitamin E concentration was below the normal range in all groups but was unaffected by selenium status. Measurements of plasma malondialdehyde revealed no difference between subjects from Dechang and subjects from Mianning. Selenium supplementation raised plasma glutathione peroxidase activity and plasma selenium concentration in all groups. Groups with higher plasma selenium concentration had relatively smaller increases in glutathione peroxidase activity than in selenium concentration. These results characterize the selenium deficiency in subjects at risk for developing Keshan disease. The results obtained with supplementation of selenium indicate the presence of additional plasma forms of selenium besides glutathione peroxidase.

Effect of selenium deficiency on hydroperoxide-induced glutathione release from the isolated perfused rat heart.

Selenium deficiency has been implicated as a cause of the cardiomyopathy known as Keshan disease in China. Selenium is an essential constituent of glutathione peroxidase, an enzyme that destroys hydroperoxides by using the reducing equivalents of reduced glutathione (GSH). We studied glutathione-dependent hydroperoxide metabolism in isolated perfused rat hearts. Hearts from selenium-deficient rats contained 5% of the glutathione peroxidase activity found in control hearts. Glutathione reductase activity and glutathione content were not affected by selenium deficiency. Infusion of t-butylhydroperoxide into control hearts caused an increase in heart glutathione disulfide (GSSG) concentration proportional to the rate of hydroperoxide infusion up to 200 nmol/(g heart X min). GSSG was released into the perfusate in proportion to the hydroperoxide infusion rate up to 150 nmol/(g heart X min), but GSSG release did not increase further with higher infusion rates. Thus, GSSG release by the heart is saturable. It had a maximum rate of about 14 nmol GSH equivalents/(g heart X min) when stimulated by t-butylhydroperoxide infusion. This indicates that GSSG release by the heart is carrier-mediated and is not due to passive diffusion. Infusion of hydroperoxide into selenium-deficient hearts failed to cause increases in heart GSSG concentration and in GSSG release. This indicates that selenium-deficient heart cannot metabolize hydroperoxides through glutathione-dependent pathways. We suggest that selenium deficiency might predispose the heart to injury from oxidant stress.