Dietary Selenium Deficiency or Excess Reduces Sperm Quality and Testicular mRNA Abundance of Nuclear Glutathione Peroxidase 4 in Rats

Abstract

Glutathione peroxidase (GPX) 4 and selenoprotein P (SELENOP) are abundant, and several variants are expressed in the testis. We determined the effects of dietary selenium deficiency or excess on sperm quality and expressions of GPX4 and SELENOP variants in rat testis and liver. After weaning, male Sprague-Dawley rats were fed a Se-deficient basal diet (BD) for 5 wk until they were 9 wk old [mean ± SEM body weight (BW) = 256 ± 5 g]. They were then fed the BD diet alone (deficient) or with 0.25 (adequate), 3 (excess), or 5 (excess) mg Se/kg for 4 wk. Testis, liver, blood, and semen were collected to assay for selenoprotein mRNA and protein abundances, selenium concentration, GPX activity, 8-hydroxy-deoxyguanosine concentration, and sperm quality. Dietary selenium supplementations elevated ( < 0.05) tissue selenium concentrations and GPX activities. Compared with those fed BD + 0.25 mg Se/kg, rats fed BD showed lower ( < 0.05) BW gain (86%) and sperm density (57%) but higher ( < 0.05) plasma 8-hydroxy-deoxyguanosine concentrations (189%), and nonprogressive sperm motility (4.4-fold). Likewise, rats fed BD + 5 mg Se/kg had ( = 0.06) lower BW gain and higher (1.9-fold) sperm deformity rates than those in the selenium-adequate group. Compared with the selenium-adequate group, dietary selenium deficiency (BD) or excess (BD + 3 or 5 mg Se/kg) resulted in 45-77% lower ( < 0.05) nuclear () mRNA abundance in the testis. Rats fed BD had lower ( < 0.05) mRNA levels of 2 variants in both testis and liver than those in the other groups. Testicular SELENOP was 155-170% higher ( < 0.05) in rats fed BD + 5 mg Se/kg and hepatic c/mGPX4 was 13-15% lower ( < 0.05) in rats fed BD than in the other groups. The mRNA abundance of rat testicular nGPX4 responded to dietary selenium concentrations in similar ways to sperm parameters and may be used as a sensitive marker to assess appropriate Se status for male function.

The GC2 haplotype of the vitamin D binding protein is a risk factor for a low plasma 25-hydroxyvitamin D concentration in a Han Chinese population

“…Participants, randomly recruited over one year at a health examination centre in Shenzhen City, were informed of the purpose of the questionnaire, physical examination, and blood sampling, and they provided their written consent. Health history and food intake data were collected via face-to-face interviews using a computerized version of the questionnaire applied in China’s 2010 Chronic Disease and Risk Factor Surveillance [33], into which questions regarding sunshine exposure and sun protection use (collected by 3 categorized values: 1 = never use; 2 = use always under sunshine; and 3 = use only under strong sunlight) were incorporated. VD intakes were calculated using the dietary VD concentration data published by the US Department of Agriculture (USDA Nutrient Database for Standard Reference, Release 28.…”

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

“…Following a two-week adaptation period, mice were randomly divided (n = 18 each) into five groups i.e., Group 1, Group 2, Group 3, Group 4, and Group 5. At the start of an 8-week feeding trail, mice in all groups were fed a Se-deficient (Se-D) diet (sodium selenite 0.08 mg Se/kg) for initial two weeks to adapt to the experimental diets and to deplete their Se stores to equate the baseline blood Se status [53]. For the next six weeks, mice in different groups (Groups 1-5) were retagged as Se-deficient (Se-D), inorganic Se-adequate (ISe-A), inorganic Se-supplemented (ISe-S), organic Se-adequate (OSe-A), and organic Se-supplemented (OSe-S) groups, respectively.…”

Role of glutathione peroxidase 1 in glucose and lipid metabolism-related diseases

“…Dietary Se deficiency decreased GPX1 gene and protein expression in different tissues of several mammalian species [24–35]. While the deficiency did not affect body weights of mice [36], it decreased blood glucose concentration and hepatic concentrations of total cholesterol (TC), triglyceride (TG), and nonesterified free fatty acid (NEFA) in 5-month old mice [13, 15, 37], compared with the Se-adequate controls.…”

“…Although GPX1 mRNA, protein, and activity were highly responsive to dietary Se changes in different tissues of various species [25, 29, 30, 33–35, 42, 63], its mRNA was not changed by a high-fat diet in the heart, hypothalamus, kidney, liver, muscle, pancreas, perirenal adipose tissue (PAT), pituitary, subcutaneous adipose tissue (SAT), or thyroid [64, 65] of pigs. However, several other selenoprotein genes including DIO2 , SELENOI , SELENOS , SELENOV , and TXNRD1 in the thyroid; SELENOF in the liver; SELENOO in the kidney; GPX4 , GPX6 , DIO1 , and SELENOV in the muscle; GPX4 and SELENOM in the pituitary; and GPX3 in the hypothalamus were up-regulated by the high fat diet in pigs.…”