Cisplatin cytotoxicity is dependent on mitochondrial respiration in .

Objectives: To understand the role of mitochondrial respiration in cisplatin sensitivity, we have employed wild-type and mitochondrial DNA depleted Rho0 yeast cells.

Materials And Methods: Wild type and Rho0 yeast cultured in fermentable and non-fermentable sugar containing media, were studied for their sensitivity against cisplatin by monitoring growth curves, oxygen consumption, pH changes in cytosol/mitochondrial compartments, reactive oxygen species production and respiratory control ratio.

Results: Wild-type yeast grown on glycerol exhibited heightened sensitivity to cisplatin than yeast grown on glucose.

Intracellular zinc status influences cisplatin-induced endothelial permeability through modulation of PKCα, NF-κB and ICAM-1 expression.

Platinum-based chemotherapeutic regimen induces vascular dysfunction. Action of cisplatin on endothelial cells is mediated by protein kinase C (PKC-α), which further activates nuclear factor-κB (NF-κB) and induces canonical transient receptor potential channel (TRPC1) and intercellular adhesion molecule (ICAM-1) expression. Increased ICAM-1 contributes to hyperadhesion of monocytes and endothelial dysfunction.

Attenuation of non-enzymatic thermal glycation of bovine serum albumin (BSA) using β-carotene.

Although heat treatment of proteins is believed to promote and accelerate glycation, the accompanying structural changes in proteins because of heat denaturation and/or glycation are not completely understood. In addition, there is an increasing interest for inhibitors of thermal glycation in food processing. β-Carotene is a naturally occurring carotenoid found in many vegetables, fruits and herbs, with known antioxidant activity.