Exposure to UV light triggers the rapid generation and accumulation of reactive oxygen species (ROS) in skin cells, with consequent increase in oxidative stress and thus in photoaging. Exogenous supplementation with dietary antioxidants and/or skin pretreatment with antioxidant‐based lotions before sun exposure might be a winning strategy against age‐related skin pathologies. In this context, plants produce many secondary metabolites to protect themselves from UV radiations and these compounds can also protect the skin from photoaging. Phenolic compounds, ascorbic acid and carotenoids, derived from different plant species, are able to protect the skin by preventing UV penetration, reducing inflammation and oxidative stress, and influencing several survival signalling pathways. In this review, we focus our attention on the double role of oxidants in cell metabolism and on environmental and xenobiotic agents involved in skin photoaging. Moreover, we discuss the protective role of dietary antioxidants from fruits and vegetables and report their antiaging properties related to the reduction of oxidative stress pathways.

Metabolic control is mediated by the dynamic assemblies and function of multiple redox enzymes. A key element in these assemblies, the P450 oxidoreductase (POR), donates electrons and selectively activates numerous (>50 in humans and >300 in plants) cytochromes P450 (CYPs) controlling metabolism of drugs, steroids and xenobiotics in humans and natural product biosynthesis in plants. The mechanisms underlying POR-mediated CYP metabolism remain poorly understood and to date no ligand binding has been described to regulate the specificity of POR. Here, using a combination of computational modeling and functional assays, we identify ligands that dock on POR and bias its specificity towards CYP redox partners, across mammal and plant kingdom. Single molecule FRET studies reveal ligand binding to alter POR conformational sampling, which results in biased activation of metabolic cascades in whole cell assays. We propose the model of biased metabolism, a mechanism akin to biased signaling of GPCRs, where ligand binding on POR stabilizes different conformational states that are linked to distinct metabolic outcomes. Biased metabolism may allow designing pathway-specific therapeutics or personalized food suppressing undesired, disease-related, metabolic pathways.