Osmotic Effects on Fatty Acid, Pyruvate, and Ketone Body Oxidation in Oyster Gill Mitochondria

Abstract

The effects of osmolarity on oxidation of fatty acyl carnitines, pyruvate, and ketone bodies were examined in gill mitochondria from oysters (Crassostrea virginica) acclimated to full-strength seawater (FSW) and dilute seawater (DSW). In gill mitochondria from FSW oysters, oxidation of pyruvate was stimulated twofold by hypoosmotic incubation. Oxidation of acetoacetate and beta-hydroxybutyrate was not affected by hypoosmotic incubation. No stimulation of oxidation of C-2 or C-6 fatty acyl carnitines occurred, but oxidation of octanoyl carnitine (C-8) was stimulated by approximately 75%. Oxidation of other medium-chain fatty acyl carnitines (C-10-C-14) and longchain fatty acyl carnitines (C-16, C-18) was stimulated fourfold by hypoosmotic incubation. The stimulation of fatty acyl carnitine oxidation in response to hypoosmotic incubation was due to changes in osmolarity, not to assay medium ionic strength. Without exception, the stimulatory effects of incubation in hypoosmotic medium could be duplicated by acclimation to DSW with subsequent incubation in an isosmotic medium, indicating that osmotic effects on mitochondrial metabolite oxidation are due to changes in the matrical milieu. The physiological significance of these findings are discussed in relation to energy and solute metabolism during osmotic stress in bivalve molluscs.