ABSTRACT

Extensive research in the last few years has revealed that the regular consumption of certain fruits containing carotenoids, an important group of phytochemicals derived from such fruits and vegetables, is involved in cancer prevention. Both prospective and retrospective epidemiological studies have consistently and clearly shown that an increased intake of fruits and vegetables rich in carotenoids is associated with a decreased risk of cancer (Mayne, 1996; Peto

et al., 1981; Ziegler et al., 1996). Accordingly, a number of in vitro and in vivo studies reported that b-carotene and other carotenoids inhibit the growth of cancer cells (Gerster, 1995, Palozza, 2005; Palozza et al., 2004b, 2006a). In particular, carotenoids have been reported to attenuate or delay chemical-or ultraviolet (UV)-induced carcinogenesis in animal models. They have been also found to act as potent growth-inhibitory agents in several tumor cells, including colon, melanoma, prostate, oral, lung, and breast cancer cells and to enhance the cytotoxicity of well-known chemotherapeutics (Palozza et al., 2006a). Anticarcinogenic activities have been demonstrated for both provitamin A and nonprovitamin A carotenoids (Krinsky, 1993). In human mammary epithelial cells, morphologic changes suggesting differentiation were observed to accompany a reduced proliferative capacity in response to both b-carotene and canthaxanthin (Rock et al., 1995). Recently, carotenoids have been found to modulate several pathways of the apoptotic process (Palozza et al., 2004b). In contrast, results from human intervention studies, the b-Carotene and Retinol Ef cacy Trial (CARET) (Omenn et al., 1996) and the a-Tocopherol, b-Carotene Cancer Prevention Study (ATBC) (the a-tocopherol, Beta-Carotene Cancer Prevention Study Group, 1994), indicated that the exposure of subjects taking supplemental b-carotene to cigarette smoke increased lung cancer incidence. The Australian Polyp Study also showed that b-carotene supplementation was associated with higher risk of recurrence of large colorectal adenomas (Wahlqvist et al., 1994). In view of these contradictory ndings, there has been considerable interest in elucidating the mechanism(s) by which carotenoids affect cell growth.