Effects of dexamethasone on carnitine metabolism in liver and extrahepatic tissues

The in vivo effects of dexamethasone administration on liver and extrahepatic tissue carnitine concentrations were assessed in 48-h-starved rats. In heart and kidney, but not in liver, dexamethasone significantly increased total carnitine concentration. Acute (2.5 h) treatment with 2-tetradecylglycidate (TDG), a specific inhibitor of carnitine palmitoyl transferase 1, not only increased total hepatic carnitine concentrations, but also permitted an effect of dexamethasone (a further increase in hepatic carnitine concentration). The results are discussed in terms of acute (substrate-mediated) and chronic (hormonal) control of carnitine turnover.     

Dexamethasone induces irreversible G1 arrest and death of a human lymphoid cell line.

Growth of a human leukemic T-cell line (CEM C7) in 10(-6) M dexamethasone results in inhibition of growth and rapid loss of cell viability after a delay of approximately 18 to 24 hours. Analysis of dexamethasone-treated cells by flow-microfluorometry showed that they were arrested in the G1 phase of the cell cycle. Loss of cell viability began at the same time as G1 accumulation was first detectable, and 20% of all cells were found to be blocked in G1 at this time suggesting that loss of viability and G1 arrest were coincident events. Half-maximal and maximal effects on both viability and G1 arrest after 48 hours in steroid were nearly identical with respect to steroid concentration and corresponded to half-maximal and full occupancy of glucocorticoid specific receptor by hormone, consistent with a glucocorticoid receptor mediated mechanism for both phenomena. Most non-viable cells were arrested in G1, and accumulation of cells in G1 was irreversible; removal of steroid in the presence of colcemid did not result in a decreased fraction of G1 cells. Furthermore, dexamethasone treatment did not protect cells against the effects of 33258 Hoechst-amplified killing of bromodeoxyuridine substituted cells exposed to light. These results show that dexamethasone arrests these leukemic cells in G1 and strongly suggest that dexamethasone-treated cells are killed upon entry into G1.     

A regional localisation for an X-linked suppressor gene (XS) for the Lutheran blood group

Summary Suppression of Lutheran blood group expression is usually associated with an autosomal dominant suppressor gene In(Lu) which results in the rare Lu(a-b-) phenotype. X-linked recessive suppression can also occur under the control of the XS locus with normal (XS1) and suppressor (XS2) alleles. The only known kindred with XS2 segregating was examined for polymorphic DNA markers with known regional localisations on the X chromosome. Two point linkage analysis suggested linkage of XS to DXS14 (p58.1) with =0.00, =1.96. DXS14 is situated near the centromere at Xp11. Recombinants with DXS84 (distal to DXS14 on Xp) and recombinants with DXYS1 (pDP34) (on the proximal part of Xq) suggests a localisation for XS near the centromere, between DXS84 and DXYS1 (Xp21.2-Xq21.1). Linkage to a marker on the X chromosome confirms the original assignment of XS to the X chromosome, which was based on pedigree inspection from this family.