INTRODUCTION: Oxidative stress is one of the risk factors of colorectal carcinogenesis. In inflammatory reactions the activated leucocytes product mutagenic and mitogenic free radicals, hereby promoting tumor formation. Obesity, hyperlipidemia and hyperinsulinemia increases the energy supply of epithelial cells, thus leads to deregulation of mitochondrial electron transport chain. The latter leads to increased free radical production that causes troubles in cell cycle regulation, mutations, and unrestricted proliferation of damaged cells. AIM: Evaluation of some parameters of antioxidant and nutritional status in patients with benign or malignant colorectal neoplasm. METHODS: Assessment of nutrient intake, measurement of some anthropometric parameters (body height, body weight, waist, hip and arm circumference, waist/hip ratio), determination of serum prealbumin level, evaluation of the biomarkers of antioxidant status (superoxide dismutase and glutathione peroxidase activity, levels of uric acid and albumin, total antioxidant status, free radical scavenger capacity), determination the concentration of oxidated product and malondialdehyde. RESULTS: In patients with malignant tumor the dietary fiber, folate and vitamin A intake was under the optimal level, and the serum prealbumin concentration was lower than in patients with benign lesion. There was a high incidence of overweight and obesity among patients. Significant difference was found between diseased subjects and healthy controls in terms of the biomarkers of antioxidant status, such as free radical scavenger capacity, concentration of advanced oxidation protein products and malondialdehyde, glutathione peroxidase activity. CONCLUSIONS: The insufficient folate and vitamin A intake, the high incidence of overweight and obesity, and the abnormal values of the biomarkers of antioxidant status observed in the study groups seem to support the correlation between colorectal tumor, nutritional and antioxidant status.
INTRODUCTION: Oxidative stress is one of the risk factors of colorectal carcinogenesis. In inflammatory reactions the activated leucocytes product mutagenic and mitogenic free radicals, hereby promoting tumor formation. Obesity, hyperlipidemia and hyperinsulinemia increases the energy supply of epithelial cells, thus leads to deregulation of mitochondrial electron transport chain. The latter leads to increased free radical production that causes troubles in cell cycle regulation, mutations, and unrestricted proliferation of damaged cells. AIM: Evaluation of some parameters of antioxidant and nutritional status in patients with benign or malignant colorectal neoplasm. METHODS: Assessment of nutrient intake, measurement of some anthropometric parameters (body height, body weight, waist, hip and arm circumference, waist/hip ratio), determination of serum prealbumin level, evaluation of the biomarkers of antioxidant status (superoxide dismutase and glutathione peroxidase activity, levels of uric acid and albumin, total antioxidant status, free radical scavenger capacity), determination the concentration of oxidated product and malondialdehyde. RESULTS: In patients with malignant tumor the dietary fiber, folate and vitamin A intake was under the optimal level, and the serum prealbumin concentration was lower than in patients with benign lesion. There was a high incidence of overweight and obesity among patients. Significant difference was found between diseased subjects and healthy controls in terms of the biomarkers of antioxidant status, such as free radical scavenger capacity, concentration of advanced oxidation protein products and malondialdehyde, glutathione peroxidase activity. CONCLUSIONS: The insufficient folate and vitamin A intake, the high incidence of overweight and obesity, and the abnormal values of the biomarkers of antioxidant status observed in the study groups seem to support the correlation between colorectal tumor, nutritional and antioxidant status.
Authors: Bochra Gargouri; Jos Van Pelt; Abd El Fatteh El Feki; Hammadi Attia; Saloua Lassoued Journal: Mol Cell Biochem Date: 2008-12-11 Impact factor: 3.396