Inhibition of benzoyl peroxide and ultraviolet-B radiation induced oxidative stress and tumor promotion markers by cycloartenol in murine skin.
The chemopreventive potential of cycloartenol on benzoyl peroxide and UVB radiation-induced cutaneous tumor promotion markers and oxidative stress in murine skin is assessed. Benzoyl peroxide treatment (20 mg/animal/0.2 ml acetone) and UVB radiation (0.420 J/m(2)/s) caused a decrease in the activities of cutaneous antioxidant enzymes namely, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, phase II metabolizing enzyme such as glutathione-S-transferase and quinone reductase and depletion in the level of cutaneous glutathione. There was also enhancement in cutaneous microsomal lipid peroxidation, xanthine oxidase activity, [(14)C]-ornithine decarboxylase activity and [(3)H]-thymidine incorporation into cutaneous DNA. Cycloartenol was topically applied prior to the application of benzoyl peroxide at dose levels of 0.2 mg and 0.4 mg/kg body weight in acetone, which resulted in significant inhibition of epidermal ornithine decarboxylase activity and DNA synthesis (P < 0.001). There was also significant reduction of lipid peroxidation and xanthine oxidase activity (P < 0.001). In addition, the depleted levels of glutathione, inhibited activities of antioxidant and phase II metabolizing enzymes, were also recovered to a significant level (P < 0.001). The data indicate that cycloartenol is an effective chemopreventive agent in skin carcinogenesis.
Sultana
Sarwat
S
Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), New Delhi, India. sarwat786@rediffmail.com
Alam
Aftab
A
Khan
Naghma
N
Sharma
Sonia
S
D000818:Animals; D016588:Anticarcinogenic Agents / Q000737:chemistry / Q000627:therapeutic use*; D001585:Benzoyl Peroxide / Q000494:pharmacology*; D014408:Biomarkers, Tumor; D002374:Catalase / Q000096:biosynthesis; D003600:Cytosol / Q000378:metabolism; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000096:biosynthesis; D005978:Glutathione / Q000096:biosynthesis / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000096:biosynthesis; D005980:Glutathione Reductase / Q000096:biosynthesis; D005982:Glutathione Transferase / Q000096:biosynthesis; D015227:Lipid Peroxidation; D051379:Mice; D008861:Microsomes / Q000378:metabolism; D009381:Neoplasms, Radiation-Induced; D018384:Oxidative Stress; D010840:Phytosterols / Q000737:chemistry / Q000627:therapeutic use*; D012867:Skin / Q000187:drug effects / Q000378:metabolism; D012878:Skin Neoplasms / Q000517:prevention & control*; D013347:Subcellular Fractions / Q000378:metabolism; D014315:Triterpenes; D014466:Ultraviolet Rays; D014969:Xanthine Oxidase / Q000378:metabolism
D016588:Anticarcinogenic Agents; D014408:Biomarkers, Tumor; D010840:Phytosterols; D014315:Triterpenes; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D014969:Xanthine Oxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D001585:Benzoyl Peroxide; C100089:cycloartenol