Zhou Q, Kummerow F A
Burnsides Research Laboratory, University of Illinois, Urbana 61801, USA.
Magnes Res. 1995 Jun;8(2):145-50.
This study investigated the effects of magnesium deficiency on thymidine incorporation and lipid synthesis in human umbilical arterial endothelial cells. To study [3H]thymidine incorporation, the cells were exposed for 12 to 96 h to experimental media containing decreasing magnesium concentrations of 237, 118 and 5 microM. A magnesium concentration of 949 microM was used as control. At 48 h of exposure to the experimental media, magnesium was restored to 949 microM in half of the magnesium-deficient cultures. To determine [14C]acetic acid distributions among cholesterol, phospholipid and triglyceride, the cells were treated with decreased magnesium media at the levels mentioned above for 12 to 48 h. The results showed that [3H]thymidine incorporation into DNA was inhibited by magnesium deficiency. The inhibition was augmented correspondingly with decreased magnesium concentrations and increased exposure periods. When magnesium in the medium was enhanced to normal level, incorporation was no longer inhibited. Incorporation of [14C]acetic acid into phospholipid was inhibited, its incorporation into triglyceride was stimulated, but its incorporation into cholesterol was not affected by magnesium deficiency. We suggest (i) that with the restoration of adequate magnesium, the inhibiting effect of magnesium deficiency on thymidine incorporation is reversible; (ii) that magnesium deficiency can result in a redistribution of [14C]acetic acid between phospholipid and triglyceride.
