-
[show abstract]
[hide abstract]
ABSTRACT: Reactive oxygen species (ROS) are associated not only with initiation, but also with promotion and progression in the multistage carcinogenesis model. In the present review, we will focus on the involvement of ROS in skin carcinogenesis, especially that induced by ultraviolet (UV) radiation. UV-specific DNA damage has been well studied thus far. However, recent reports have revealed the previously unknown participation of oxidative stress in UV-induced skin carcinogenesis. Indeed, in addition to transition-type mutations at dipyrimidine sites, G:C to T:A transversions, which may be induced by the presence of 8-oxoguanine during DNA replication, are frequently observed in the ras oncogene and p53 tumor suppressor gene in human skin cancers of sun-exposed areas and in UV-induced mouse skin cancers. Recent studies have shown that not only UV-B, but also UV-A is involved in UV-induced carcinogenesis. A wide variety of biological phenomena other than direct influence by UV, such as inflammatory and immunological responses and oxidative modifications of DNA and proteins, appear to play roles in UV-induced skin carcinogenesis. Furthermore, it has become clear that genetic diseases such as xeroderma pigmentosum show deficient repair of oxidatively modified DNA lesions. The involvement of ROS in skin carcinogeneisis caused by arsenic and chemical carcinogens will also be discussed.
Antioxidants and Redox Signaling 07/2004; 6(3):561-70. · 8.46 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Abstract Photoaging is significantly different from chronological aging in both clinical and histological appearance. It has been suggested that oxidative stress, generated by ultraviolet radiation (UVR), leads to photoaging over a long period. The presence of 8-OHdG, and oxidatively modified proteins such as 4-hydroxy-2-nonenal-modified protein, 3-l-nitro-tyrosine and N–ε(carboxymethyl)lysine in UV-exposed skin specimens, supports this theory. The pathophysiology of photoaging of the skin caused by chronic inflammation after UVR is reviewed and discussed, with a focus on oxidative stress.
Experimental Dermatology 11/2003; 12(s2):18 - 21. · 3.54 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Photoaging is significantly different from chronological aging in both clinical and histological appearance. It has been suggested that oxidative stress, generated by ultraviolet radiation (UVR), leads to photoaging over a long period. The presence of 8-OHdG, and oxidatively modified proteins such as 4-hydroxy-2-nonenal-modified protein, 3-L-nitro-tyrosine and N(-epsilon) (carboxymethyl)lysine in UV-exposed skin specimens, supports this theory. The pathophysiology of photoaging of the skin caused by chronic inflammation after UVR is reviewed and discussed, with a focus on oxidative stress.
Experimental Dermatology 02/2003; 12 Suppl 2:18-21. · 3.54 Impact Factor
