Abstract

Opuntia humifusa, member of the Cactaceae family, was previously demonstrated to have radical scavenging, anti-inflammatory and anti-proliferative effects in in vitro models. It was suggested that O. humifusa could function in the prevention of carcinogenesis. To investigate the in vivo chemopreventive effect of O. humifusa, mice were fed a diet containing either 1% or 3% following 7, 12-dimethylbenz[a] anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA) induction of skin carcinogenesis. Significant decrease in the numbers of papilloma and epidermal hyperplasia were observed in mice fed with O. humifusa, compared to the control group. O. humifusa also upregulated high total antioxidant capacity and level of phase II detoxifying enzyme such as superoxide dismutase and glutathione S-transferase activity in the skin. Lipid peroxidation activity level was measured in skin cytosol and significantly inhibited in 3% OH fed group compared to the control group. These results suggest that O. humifusa exerts chemopreventive effects on chemical carcinogenesis in mouse skin and that prevention effects are associated with reduction of oxidative stress via the modulation of cutaneous lipid peroxidation, enhancing of total antioxidant capacity especially in phase II detoxifying enzyme system and partial apoptotic influence.

Highlights

  • Skin cancer is the most frequently diagnosed cancer and represents an important public health problem due to its high incidence and medical costs (Hara-Chikuma et al, 2008)

  • These results suggest that O. humifusa exerts chemopreventive effects on chemical carcinogenesis in mouse skin and that prevention effects are associated with reduction of oxidative stress via the modulation of cutaneous lipid peroxidation, enhancing of total antioxidant capacity especially in phase II detoxifying enzyme system and partial apoptotic influence

  • During the tumor promotion stage, repeated application of TPA can trigger the production of squamous papilloma and epidermal hyperplasia, which is the pre-neoplastic lesion of skin carcinoma (Shelton et al, 2000; Abel et al, 2009)

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Summary

Introduction

Skin cancer is the most frequently diagnosed cancer and represents an important public health problem due to its high incidence and medical costs (Hara-Chikuma et al, 2008). Under a sustained environmental stress, ROS are over-produced for a long time and can be an important source of damage to cell structures, including lipids and membranes, proteins and nucleic acids, result in oxidative stress (Poli et al, 2004; Fang et al, 2009; Khandrika et al, 2009). The accumulation of oxidative stress during the life cycle accelerates the DNA mutations or induces DNA damage, genome instability and cell proliferation (Halliwell et al, 2007; Parmar et al., 2010). This repeated active oxidative damage has been linked to all three stages of tumor development, i.e., initiation, promotion and progression (Scandalios et al, 2005; Visconti et al, 2009). Reducing intracellular oxidative stress or blocking ROS generation may represent an effective strategy for preventing skin carcinogenesis

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