The processes of aging and photoaging are associated with an increase in cellular oxidation. This may be in part due to a decline in the levels of the endogenous cellular antioxidant coenzyme Q10 (ubiquinone, CoQ10). Therefore, we have investigated whether topical application of CoQ10 has the beneficial effect of preventing photoaging. We were able to demonstrate that CoQ10 penetrated into the viable layers of the epidermis and reduce the level of oxidation measured by weak photon emission. Furthermore, a reduction in wrinkle depth following CoQ10 application was also shown. CoQ10 was determined to be effective against UVA mediated oxidative stress in human keratinocytes in terms of thiol depletion, activation of specific phosphotyrosine kinases and prevention of oxidative DNA damage. CoQ10 was also able to significantly suppress the expression of collagenase in human dermal fibroblasts following UVA irradiation. These results indicate that CoQ10 has the efficacy to prevent many of the detrimental effects of photoaging.

Programmed death of cells by apoptosis is regarded as a protective mechanism of the organism against an accumulation and spread of defective cells. The rate of apoptosis is elevated in most types of aging cell populations. However, there are also findings about a decreased susceptibility of senescent cells in vivo and in vitro, particularly to apoptosis induced by oxidative and energetic stress. Mitochondria appear to have a key function in apoptosis regulation. Thus, apoptosis can be induced by defective mitochondrial oxidative phosphorylation. The role of apoptosis in aging and age-related disease was outlined for different organs (brain, cardio-vascular system, immune system, intestine, macula of the eye, Langerhans islets, prostate gland, oocytes of ovaries). The age-related intensification of this dismantling system of cells seems to highlight the deterioration of tissue and organ structure and function in aging.

The activity of antioxidant enzymes and the concentration of the lipid peroxidation product malondialdehyde (MDA) as indicator of oxidative damage were determined in selected tissues of healthy mice and transplanted B16 melanoma-bearing mice with increasing age. A total of 60 male mice were divided into 6 groups. Groups 1, 2 and 3 consisted of tumor-free, healthy mice aged 1, 9 and 16 months, respectively (average life span: 2 years). Groups 4, 5 and 6 consisted of mice of the same age as the healthy mice, but given intraperitoneally 10(6) cells of B16 melanoma for 2 weeks. An increase in the concentration of MDA was found in all the studied tissues (brain, liver, lungs, erythrocytes) and blood plasma of 16-month old healthy mice compared with the younger ones. The activity of superoxide dismutase (SOD) and catalase (CAT) was elevated in the brain and the activity of CAT and glutathione peroxidase (GPx) in the liver of aged healthy mice. The transplantation of melanoma caused an increase of the concentration of MDA and of the activity of all studied enzymes in all tissues. This elevation was most pronounced in the youngest mice group 4 and was higher than in the oldest healthy group 3. Thus, these early changes of the "(anti-)oxidative status" in the investigated tissues caused by the tumor development have similarities with age-associated alterations of healthy mice, especially in regard to MDA in all tissues or SOD and CAT in brain.

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