Menadione-induced oxidative stress in bovine heart microvascular endothelial cells.

Objective: Oxidative stress from increased production of reactive oxygen species or decreased efficiency of inhibitory and scavenger systems may contribute to vascular injury. In this study, we developed an in vitro model of vascular injury by menadione-induced oxidative stress in bovine heart microvascular endothelial cells.

Methods: Oxidative stress was induced by exposure to menadione.

Proteoglycan synthesis by bovine myocardial endothelial cells is increased by long-term exposure to high concentrations of glucose.

The role of the metabolic milieu in control of proteoglycan synthesis was investigated using bovine myocardial endothelial cells (BMEC) grown for six to eight passages in media containing either 5.6 or 25 mM glucose. Macromolecular Na[35S]sulfate incorporation into proteoglycans was increased by exposure to 25 mM when compared with 5.

Reverse cholesterol transport with acute exercise.

Physical activity has been shown to be inversely related to coronary heart disease (CHD). The role of high density lipoprotein (HDL) particles in the process of reverse cholesterol transport may be a link between exercise and the prevention of CHD. The aim of the present study was to evaluate the effects of acute exercise on cholesterol efflux (C-EF) from human monocyte derived macrophages overloaded with cholesterol and subsequently incubated with HDL fractions isolated from plasma.

Antioxidant potential of specific estrogens on lipid peroxidation.

Coronary heart disease (CHD) is the leading cause of death in postmenopause. Estrogen administration in postmenopause lowers the risk of CHD by 50%. A variety of estrogen preparations are currently used in postmenopausal hormone replacement therapy.