title: The effect of nutrition on chemical toxicity.
abstract: The toxicity of chemicals, and of reactive oxygen species (ROS), are both affected by nutrition and diet. Calorific excess (continuous feeding), or deficiency (fasting), may increase production of ROS, which are also formed by interaction of toxic chemicals with cytochromes P450 (CYP2E or futile cycling). Both ROS (GSH reductase and peroxidase) and toxic chemicals (S-transferases) are detoxified by GSH enzymes; ROS are scavenged by a system comprising GSH, ascorbic acid and tocopherols, which may be regenerated by NADPH. Dietary protein is necessary for GSH or enzyme replacement, lipids are required for polyunsaturated fatty acids (PUFAs) and prostanoid biosynthesis, lipotropes and phospholipids for synthesis of endoplasmic reticulum, and folate is needed for dug metabolizing activity. Among required minerals, Se is necessary as the essential component of the antioxidant enzyme, glutathione peroxidase. Other dietary factors considered are the natural toxicants, gossypol, lathyrogens, glucosinolates, and saponins, and toxicants from food spoilage, food intoxication and food processing.
authors.forename: D V
authors.initials: DV
authors.lastname: Parke
authors.forename: M S
authors.initials: MS
authors.lastname: Dhami
authors.forename: M
authors.initials: M
authors.lastname: Afzal
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004032:Diet / Q000009:adverse effects*; D005506:Food Contamination; D006801:Humans; D009747:Nutritional Physiological Phenomena; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species