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A. Klein, A. W.-L. Chan and A. Malkin


Mononuclear cell preparations are capable of metabolizing cortisol to three metabolites which lack the immunosuppressive effect of their precursor. In the present study we noted a linear correlation, up to a point, between glucose concentration and the rate of human mononuclear cell cortisol metabolism in vitro. The mechanism by which glucose exerts its effect was investigated further. We observed that: (1) the effect of glucose on mononuclear cell cortisol metabolism was not influenced by insulin; (2) NADPH and NADH enhanced cortisol metabolism by disrupted cells, irrespective of whether the homogenates were dialysed or not; (3) lactate and ATP inhibited mononuclear cell cortisol metabolism and (4) almost all the glucose used was converted to lactate. It is concluded that mononuclear cell cortisol metabolism can depend on both nucleotides.

J. Endocr. (1986) 109, 181–185

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A. Klein, B. Bruser, J. B. Robinson, P. H. Pinkerton and A. Malkin


We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g. thymocytes) metabolize cortisol at a different rate from cortisol-resistant cells and whether lymphocytes in which cortisol catabolism is inhibited become cortisol sensitive. The work was facilitated by the observation that an ethanol extract plasma from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) had the capacity to inhibit CCL.

The capacity of thymocytes to metabolize cortisol was found to be 11 times lower than that of peripheral lymphocytes. Inhibition of CCL with an ethanol extract of plasma from AIDS/ARC patients made the cells vulnerable to cortisol, causing them to die at a rate seven times greater than that of control samples. It is suggested that these findings may have important implications with regard to the nature of lymphocyte depletion in AIDS/ARC patients or in people at risk of developing the syndrome.

J. Endocr. (1987) 112, 259–264