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Over the full range of all 100 cells, a mean value of 77.03 ± 21.48 fg iodine/cell ( 2.6 × 10 SP -4 sp ± 0.73 ng Q SB 10 sb /cell) was calculated, with a median value of 49.13 fg iodine/cell ( 1.66 × 10 SP -4 sp ng Q SB 10 sb /cell). Control measurements using free iodine, experiments of I SB 2 sb -Q SB 10 sb bioavailability via LC-MS/MS as well as the scans around the cell pellets clearly indicate that the measured iodine masses can only be related to the I SB 2 sb -Q SB 10 sb . (a) 26.7 ng total iodine mass in cell pellet from donor 1, (b) 28.8 ng total iodine mass in cell pellet from donor 2, (c) 27.4 ng total iodine mass in cell pellet from donor 3, (d) no iodine signal in untreated cell sample. The total reconstructed iodine masses in the capillaries were 26.7 ± 4.0 ng, 28.8 ± 4.3 ng and 27.4 ± 4.1 ng for donor 1 (600,000 cells), 2 (600,000 cells) and 3 (400,000 cells), respectively, whereas no iodine could be detected in the untreated cell sample (750,000 cells). [Extracted from the article]

Coenzyme Q10 (CoQ10) is a key component of the mitochondrial respiratory chain and, therefore, is essential for the bioenergetics of oxidative phosphorylation. It is also endowed with antioxidant properties, and recent studies pointed out its capability of affecting the expression of different genes. In this review, we analyze the data on the mechanisms by which CoQ10 interacts with skin aging processes. The effect of CoQ10 in preserving mitochondrial function cooperates in maintaining a proper energy level, which serves to prevent the aging skin from switching to anaerobic energy production mechanisms. Furthermore, the antioxidant capacity of CoQ10 contributes to a positive effect against UV-mediated oxidative stress. Some of these effects have been assessed also in vivo, by the sensitive technique of ultraweak photoemission. Finally, CoQ10 has been shown to influence, through a gene induction mechanism, the synthesis of some key proteins of the skin and to decrease the expression of some metalloproteinase such as collagenase. These mechanisms may also contribute to preserve collagen content of the skin. [ABSTRACT FROM AUTHOR]

Cutaneous aging is characterized by a decline in cellular energy metabolism, which is mainly caused by detrimental changes in mitochondrial function. The processes involved seem to be predominantly mediated by free radicals known to be generated by exogenous noxes, e.g., solar ultraviolet (UV) radiation. Basically, skin cells try to compensate any loss of mitochondrial energetic capacity by extra-mitochondrial pathways such as glycolysis or the creatine kinase (CK) system. Recent studies reported the presence of cytosolic and mitochondrial isoenzymes of CK, as well as a creatine transporter in human skin. In this study, we analyzed the cutaneous CK system, focusing on those cellular stressors known to play an important role in the process of skin aging. According to our results, a stress-induced decline in mitochondrial energy supply in human epidermal cells correlated with a decrease in mitochondrial CK activity. In addition, we investigated the effects of creatine supplementation on human epidermal cells as a potential mechanism to reinforce the endogenous energy supply in skin. Exogenous creatine was taken up by keratinocytes and increased CK activity, mitochondrial function and protected against free oxygen radical stress. Finally, our new data clearly indicate that human skin cells that are energetically recharged with the naturally occurring energy precursor, creatine, are markedly protected against a variety of cellular stress conditions, like oxidative and UV damagein vitroandin vivo. This may have further implications in modulating processes, which are involved in premature skin aging and skin damage. [ABSTRACT FROM AUTHOR]

Coenzyme Q 10 (CoQ 10 ) is an endogenous lipophilic quinone, ubiquitous in biological membranes and endowed with antioxidant and bioenergetic properties, both crucial to the aging process. In fact, coenzyme Q 10 synthesis is known to decrease with age in different tissues including skin. Moreover, synthesis can be inhibited by 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors such as statins, that are widely used hypocholesterolemic drugs. They target a key enzymatic step along the mevalonate pathway, involved in the synthesis of both cholesterol and isoprenylated compounds including CoQ 10 .In the present study, we show that pharmacological CoQ 10 deprivation at concentrations of statins > 10000 nM triggers intracellular oxidative stress, mitochondrial dysfunction and generates cell death in human dermal fibroblasts (HDF). On the contrary, at lower statin concentrations, cells and mainly mitochondria, are able to partially adapt and prevent oxidative imbalance and overt mitochondrial toxicity. Importantly, our data demonstrate that CoQ 10 decrease promotes mitochondrial permeability transition and bioenergetic dysfunction leading to premature aging of human dermal fibroblasts in vitro .