Abstract
The inhibitory interactions of orthophosphate (P1) with the glucose-6-phosphatase system of intact microsomes derived from the livers of normal and Ehrlich-ascites-tumour-bearing mice reveal the appearance of a novel form of the T2 beta translocase component of the glucose-6-phosphatase system in tumour-stressed mice. Kinetic studies, with and without 20 mM P1, show a strictly classical competitive inhibition, with a K1,P1 of 4.2 mM, with disrupted microsomes from both control and tumour-bearing mouse liver. Inhibition was also observed with intact microsomes from livers of control mice, and contributions by both competitive and non-competitive components of inhibition were quantified by calculation of Kis,P1 and Kii,P1 values respectively. However, little inhibition was noted with intact microsomes from the livers of tumour-bearing mice. It is concluded that this novel form of T2 beta is less able to transport Pi, from the cytosol to the endoplasmic reticulum lumen, perhaps because of the tumour-related increased Km for Pi transport in this direction.