Selenium preserves keratinocyte stemness and delays senescence by maintaining epidermal adhesion.

Skin is constantly exposed to environmental factors such as pollutants, chemicals and ultra violet radiation (UV), which can induce premature skin aging and increase the risk of skin cancer. One strategy to reduce the effect of oxidative stress produced by environmental exposure is the application of antioxidant molecules. Among the endogenous antioxidants, selenoproteins play a key role in antioxidant defense and in maintaining a reduced cellular environment. Selenium, essential for the activity of selenoproteins, is a trace element that is not synthesized by organisms and must be supplied by diet or supplementation. The aim of this study is to evaluate the effect of Selenium supplementation on skin aging, especially on keratinocytes, the main cells of the epidermis. Our results demonstrate for the first time to our knowledge, the major role of Selenium on the replicative life span of keratinocytes and on aging skin. Selenium protects keratinocyte stem cells (KSCs) against senescence via preservation of their stemness phenotype through adhesion to the basement membrane. Additionally, Selenium supplementation maintains the homeostasis of skin during chronological aging in our senescent skin equivalent model. Controlled supplementation with Selenium could be a new strategy to protect skin against aging.

Bioeffects of a combination of trace elements on adipocyte biology.

The white adipose tissue plays a major role in the development of obesity and associated metabolic complications by producing a variety of pro and anti-inflammatory adipokines. Recently, studies in humans or in animals have shown a beneficial effect of certain trace elements such as zinc on insulin resistance and adipokine secretion. The aim of our study was to test the effect of a zinc-nickel-cobalt solution (ZnNiCo) on adipocyte function and to identify potential health effects of this solution in the context of obesity and associated disorders. No impact of ZnNiCo on adipogenesis was observed in 3T3-L1 cells. Gene expression in murine and human adipocytes was examined in the presence of ZnNiCo using whole genome microarrays. This transcriptomic analysis indicated that ZnNiCo affected the expression levels of genes in adipocytes under basal conditions or incubated with TNF-α and showed a down regulation of several inflammatory genes belonging to the cytokine and chemokine families (P < 0.01). These data were confirmed in mice fed with a high fat diet supplemented with ZnNiCo (P < 0.05). A modulation of NF-κB activation (evaluated by ELISA; P < 0.05) by ZnNiCo could explain at least in part these observations. The trace elements present in ZnNiCo are able to modulate the expression level of several inflammation related transcripts in adipocytes. These studies suggest that ZnNiCo could play a role in the prevention of inflammation in adipose tissue in obesity.

Symptomatic acquired zinc deficiency in at-risk premature infants: high dose preventive supplementation is necessary.

Zinc is a cofactor for several enzymes involved in many metabolisms. Zinc deficiency induces various disorders such as acrodermatitis enteropathica, either inherited or acquired. We report three cases of premature infants (24-31 wks gestational age) with low birthweight (650 to 940 g) and enteropathy, two of whom presented with necrotizing enterocolitis. All infants were fed by total parenteral nutrition. At a chronological age ranging from 73 to 80 days, all infants developed a periorificial dermatitis. Before the onset of the first signs, they had received zinc supplementation ranging from 146% to 195% of the recommended dose (400 microg/kg/day). Increased zinc supplementation over a course of 6-18 days induced a complete resolution of symptoms in all cases. No abnormality in the neurologic examination and no recurrence were observed at the end of the zinc treatment. Low birthweight premature infants with enteropathy on total parenteral nutrition are at risk of developing zinc deficiency. The usual recommended zinc supplementation is probably insufficient for those infants. A delay in the diagnosis of zinc deficiency may lead to severe complications.