Diet restriction as a protective mechanism in noncancer toxicity outcomes: A review

被引:23
作者
Ramaiah, SK
Apte, U
Mehendale, HM [1 ]
机构
[1] Univ Louisiana, Coll Pharm, Dept Toxicol, Monroe, LA 71209 USA
[2] Univ Louisiana, Coll Pharm, Louisiana Inst Toxicol, Monroe, LA 71209 USA
关键词
ad libitum feeding; alanine aminotransferase; diet restriction; equitoxic doses; gastric-mucosal injury; liver necrosis; noncancer end points; ozone-induced lung injury; proliferating cell nuclear antigen; sorbitol dehydrogenase; thioacetamide; tissue repair;
D O I
10.1080/109158100750058776
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
It is well documented that diet restriction (DR) increases life expectancy, slows aging, and decreases the incidence of a variety of age-associated diseases including cancer and chemical-induced carcinogenesis. With regard to chemical toxicity, very few studies have attempted to investigate the effects of DR on noncancer toxicity outcomes. This review summarizes the findings of how DR influences acute toxicity outcomes and mechanisms. DR-induced protection in ozone lung inflammation, acute toxicity of isoproterenol, ganciclovir-, aspirin- and acidified ethanol-induced gastric injury are discussed. Because similar physiologic mechanisms exist in humans, DR, if practiced as a life-style option, may improve quality of life in addition to accruing savings in burgeoning health care costs. Finally, these studies may be of value in boosting research in the area of pharmacology and therapeutics in developing potential therapeutic and safety assessment tools in human and veterinary medicine.
引用
收藏
页码:413 / 424
页数:12
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