Butterfat fatty acids differentially regulate growth and differentiation in Jurkat T-cells

✍ Scribed by Paolo Bergamo; Diomira Luongo; Francesco Maurano; Mauro Rossi

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 234 KB
• Volume: 96
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.20565

✦ Synopsis

Abstract

Synthetic Conjugated Linoleic Acid mixture (CLA; c9,t11; t10,c12‐18:2) has been previously shown to inhibit growth, and enhance apoptosis and IL‐2 mRNA synthesis in human lymphoblastic Jurkat T‐cells. In this study, two different butterfat types were evaluated and compared for their effects on Jurkat cell viability, oxidative stress, pro‐apoptotic activity, and cytokine synthesis: the conventionally produced butterfat (CBF), and organic butterfat (OBF) containing significantly higher amounts of c9,t11 (Rumenic Acid, RA), trans‐vaccenic acid (VA; t11‐18:1), α‐linolenic acid (ALA), and lower levels of linoleic acid (LA). Results from cell treatment with both butterfat mixtures showed comparable oxidative stress (superoxide production, intracellular GSH depletion,and lipid peroxides yield), NADPH oxidase activation, cytotoxicity (LDH release), and IL‐2 transcript level, whereas the effects of enhanced growth‐inhibitory and pro‐apoptotic activities were associated with OBF treatment. To then investigate each butterfat‐induced effect caused by RA, VA, LA, and ALA, cells were exposed to synthetic FA concentrations similar to those from the different butterfats. Higher oxidative stress (superoxide production, intracellular GSH depletion) was induced by α‐linolenic (ALA) and linoleic (LA) incubation (P < 0.01) and superoxide production was suppressed by specific PKCα inhibitor (Gö 6976) and linked to increased toxicity and IL‐2 synthesis inhibition. By contrast, cell treatment with RA increased apoptosis and IL‐2 synthesis. These results suggest that a supply of ALA and LA is responsible for BF‐induced oxidative stress via PKCα‐NADPH oxidase pathway, and that enhanced antiproliferative effects in OBF treated cells is essentially determined by RA‐induced pro‐apoptotic activity. © 2005 Wiley‐Liss, Inc.