title: Attenuation of benzoyl peroxide-mediated cutaneous oxidative stress and hyperproliferative response by the prophylactic treatment of mice with spearmint (Mentha spicata).
abstract: The modulating effect of spearmint (Mentha spicata) on benzoyl peroxide-induced responses of tumor promotion in murine skin was investigated. Benzoyl peroxide (BPO) is an effective cutaneous tumor promoter acting through the generation of oxidative stress, induction of ornithine decarboxylase activity and by enhancing DNA synthesis. BPO treatment (20 mg/animal) increased cutaneous microsomal lipid peroxidation and hydrogen peroxide generation. The activity of cutaneous antioxidant enzymes, namely catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase, was decreased and the level of cutaneous glutathione was depleted. BPO treatment also induced the ornithine decarboxylase activity and enhanced the [3H]thymidine uptake in DNA synthesis in murine skin. Prophylactic treatment of mice with spearmint extract (10, 15 and 20 mg/kg) 1 hr before BPO treatment resulted in the diminution of BPO-mediated damage. The susceptibility of cutaneous microsomal membrane to lipid peroxidation and hydrogen peroxide generation was significantly reduced (P < 0.05 ). In addition, depleted levels of glutathione, inhibited activity of glutathione dependent and antioxidant enzymes were recovered to a significant level (P < 0.01, P < 0.05 and P < 0.01, respectively). Similarly, the elevated ornithine decarboxylase activity and enhanced thymidine uptake in DNA synthesis was inhibited significantly (P < 0.05 ) in a dose-dependent manner. The protective effect of spearmint was dose dependent in all parameters. The result suggests that spearmint is an effective chemopreventive agent that may suppress BPO-induced cutaneous oxidative stress, toxicity and hyperproliferative effects in the skin of mice.
authors.affiliation: Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), New Delhi, India.
authors.forename: M
authors.initials: M
authors.lastname: Saleem
authors.forename: A
authors.initials: A
authors.lastname: Alam
authors.forename: S
authors.initials: S
authors.lastname: Sultana
mesh_terms: D000818:Animals; D001585:Benzoyl Peroxide / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D002273:Carcinogens / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D002374:Catalase / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D004247:DNA / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D019686:Lamiaceae / Q000737:chemistry*; D051379:Mice; D009955:Ornithine Decarboxylase / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000494:pharmacology; D012867:Skin / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*
chemical_list: D002273:Carcinogens; D010936:Plant Extracts; D004247:DNA; D006861:Hydrogen Peroxide; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D009955:Ornithine Decarboxylase; D005978:Glutathione; D001585:Benzoyl Peroxide