Introduction

Essiac is a tea prepared from a mixture of herbs [burdock root (Arctium lappa) (Bryson et al., 1978, Rhoads et al., 1984), sheep sorrel (Rumex acetosella) (Weber, 2004), slippery elm bark (Ulmus rubra) (Choi et al., 2002, Langmead et al., 2002, Brown et al., 2004), and turkey rhubarb (Rheum officinale) (Shah et al., 1972, Babu et al., 2003, Suresh et al., 2004)], and has been used in alternative medicine for over 50 years. Burdock root has been shown to have flavonoid-like antioxidants and polyphenols which are also strong antioxidants. Slippery elm bark has been shown to have anti-tumor, anti-inflammatory, and antioxidant activities. Sheep sorrel has demonstrated anti-inflammatory, antioxidant, anti-cancer and even antibacterial properties. The active ingredient in turkey rhubarb, anthraquinones, has been tested experimentally and found to have anti-inflammatory, anti-septic, anti-spasmodic and anti-tumor activities (Tamayo et al., 2000). The phytochemicals found in these ingredients have several possible modes of action which include: antioxidant which protects cells against oxidative damage, interference with DNA replication and antibacterial effects. Although Essiac has been used to treat a variety of conditions as diverse as allergies, hypertension, and osteoporosis, its primary use continues to be the treatment of cancer. Evidence for the efficacy of Essiac against cancer is mostly anecdotal. To date, only one clinical trial has been conducted with Essiac. The study involved patients suffering from advanced breast cancer and failed to show any benefits of Essiac consumption in those patients (Kaegi, 1998, Boon et al., 2000). Despite a lack of clinical studies reporting efficacy, 72% of the patients taking Essiac reported a positive opinion of the product (Richardson et al., 2000). Flor-Essence, a tea that is similar to Essiac, but contains four additional herbs watercress (Rorippa microphylla), blessed thistle (Carbenia benedictus), red clover (Trifolium pretense), and kelp (Hexagrammos decagrammus), did not prevent, but actually promoted DMBA-induced mammary tumor initiation in Sprague–Dawley rats (Bennett et al., 2004).

In vitro, Essiac has been shown to inhibit cell proliferation and induce differentiation in human prostate cancer cell lines (Ottenweller et al., 2004, Tai et al., 2004).

Reactive oxygen species (ROS) have been associated with pathogenic processes including carcinogenesis through direct effects on DNA directly and by acting as a tumor promoter (Kehrer, 1993, Salah et al., 1995, Wiseman and Halliwell, 1996, Vallyathan and Shi, 1997, Kong et al., 2001). Radicals have been demonstrated to be initiators of the oxidative process (Pietraforte et al., 2002), and to be involved in the development of disease (Aust et al., 1993, Stohs, 1995). Catalase, superoxide dismutase, glutathione and uric acid are examples of antioxidants produced by organisms under normal conditions as part of a defense system against ROS-mediated cellular injury. However, if this defense system is challenged or overwhelmed by excessive generation of ROS, redox imbalance or oxidative stress may occur. This can result in damage to the organism (Farber, 1988, Langard, 1990), and disease initiation (Halliwell and Gutteridge, 2000). ROS have also been shown to play an important role in carcinogenesis by damaging DNA and acting as tumor promoters (Wiseman and Halliwell, 1996, Kong et al., 2001).

While Essiac has been indicated as a cancer treatment agent its antioxidant properties have not been well defined. The present study uses radical generating systems for both hydroxyl (radical dotOH) and superoxide (O2radical dot−) radicals in order to examine Essiac’s ability to scavenge these free radicals. The radical dotOH radical was generated by the Fenton reaction between FeSO4 and H2O2 while the O2radical dot− radical was generated from the reaction of xanthine and xanthine oxidase. RAW 264.7 cells stimulated by Cr(VI) was used as a cellular source of radicals. The cells generated radicals after exposure to Cr(VI) similar to findings in other studies (Leonard et al., 2004) and Essiac was added to measure its effects on radicals produced in this system. Our study also used the Fenton reaction to generate radical dotOH radicals in order to measure lipid peroxidation, DNA damage, and the possible effects of Essiac on these systems. Major questions we wish to address in our study are: (1) What is the effect of Essiac on radical dotOH radicals? (2) What is the effect of Essiac on O2radical dot− radicals? (3) What is the effect of Essiac on radicals generated in a cellular system? (4) Can Essiac affect lipid peroxidation in a cellular system? (5) What effects does Essiac have on DNA damage caused by free radicals?