Effect of selenium on cultured bovine luteal cells.

The present study examined the possibility that selenium (Se) directly affects the corpus luteum (CL) and contributes to the maintenance of reproductive function. Primary culture of bovine CL was used to investigate this possibility. Se addition from 5 to 200 ppb elevated progesterone concentration of the culture medium in a dose-dependent manner which was associated with an increase in cell proliferation rather than an increase in progesterone production per cell, and decreased the lipid peroxide content of luteal cells. However, the luteal cells in which hormone production was increased by LH treatment, accumulated more lipid peroxide than in control incubations. The results suggest that Se is involved in the degradation of lipid peroxides which are by-products of active progesterone production by luteal cells. The increase of cell proliferation observed in this experiment was associated with the removal of these toxic peroxides.

Comparison in inducing effect on vitamin E deficiency symptoms in chicks between dilauryl succinate and unsaturated fatty acids.

Dilauryl succinate (DLS) and unsaturated fatty acids (UFA) were compared for the effects of inducing vitamin E deficiency symptoms in chicks. Experimental diets containing DLS, UFA and DLS + UFA, respectively, were given to 1-day-old chicks for 28 days. The diet containing DLS but not UFA showed far less increase in peroxide value than those containing UFA or DLS + UFA when left in a battery brooder of 30 degrees. Vitamin E deficiency symptoms in chicks given DLS + UFA were more severe than those in chicks fed either DLS or UFA. No significant difference in vitamin E deficiency symptoms except incidence of encephalomalacia was observed between the chicks given DLS and UFA. Extracting UFA from the diet containing DLS + UFA resulted in the reduction of vitamin E deficiency induction to the same degree as the diet containing DLS. Synthetic antioxidants were effective in alleviating the vitamin E deficiency symptoms in the chicks fed UFA and DLS + UFA, while only slightly effective in those given DLS. It was found that the effects of DLS and UFA can be separated and combined technically and it was suggested that they have different mechanism in inducing vitamin E deficiency.

Effect of monolauryl succinate, lauryl alcohol and succinic acid on hemolysis and liver mitochondrial lysis in vitro in chicks.

In order to elucidate the mechanism of dilauryl succinate-induced vitamin E deficiency in vivo in chicks, I conducted experiments to study the effect of the metabolites of dilauryl succinate in chicks on hemolysis and the liver mitochondrial lysis, while neither lauryl alcohol nor succinic acid induced mitochondrial lysis in vitro in chicks. These were monolauryl succinate, lauryl alcohol and succinic acid. Monolauryl succinate induced both hemolysis and mitochondrial lysis at the same concentration as that of monolauryl succinate. At the concentration of 40 times that of monolauryl succinate, lauryl alcohol induced hemolysis but succinic acid did not. Neither alpha-tocopherol, selenium nor combination of both exerted preventive effects on the reactions of monolauryl succinate or lauryl alcohol. Monolauryl succinate-induced mitochondrial lysis was not accompanied by lipid peroxidation. The observations were consistent with those in Tween 20-induced hemolysis and mitochondrial lysis, but not with those in hydrogen peroxide-induced hemolysis or with those in glutathione-induced mitochondrial lysis. It was suggested that dilauryl succinate-induced vitamin E deficiencies in vivo in chicks are mainly due to the surface activity, which is not relevant to peroxide formation, of monolauryl succinate and partly to that of lauryl alcohol.