The pathological effects of cigarette smoke (CS) have been extensively documented. The CS produces over 4,000 compounds in gaseous and particulate states that are able to induce oxidative stress to the cells.

Skin acts as a first line of defense against environmental trauma. The upper layer of the skin, the stratum corneum, is composed by a lipid barrier.The alteration of the skin lipids composition by the exposure to environmental stressors can affect the capacity of the SC to protect us from dehydration and external dangers.

Scavenger Receptor B1 (SR-B1) has been shown to be involved in the uptake of cholesterol from HDL to peripheral tissues therefore its role in skin homeostasis is crucial.

In the present work we studied the effects of CS and some of its products such as acrolein, 4HNE and H2O2 on SR-B1 expression in human keratinocytes. CS exposure decreased SR-B1 level and induced the formation of aldehydes adducts.

By contrast, cells treated with several doses of acrolein or 4HNE or H2O2 did not affect SR-B1. The treatment with glucose oxidase induces the same effect of CS as to concern SR-B1 levels and this was reversed by catalase.

In addition, CS induced the activation of NADPH oxidase measured as p67 translocation to the membrane.

The data from this study show the decreased levels of SR-B1 after CS exposure is mainly driven by the production of H2O2 (exogenous and endogenous), this could lead to the disturbance of the skin lipid barrier affecting skin physiology and be a possible cause of disorders such as skin aging and wound healing linked to CS exposure.