Dietary deficiency of calcium is widespread, so supplements as therapeutics or prophylactics for skeletal development
and osteoporosis are common. Supplements of iron, lower in the activity series, create oxidative stress (OS) in the
gastrointestinal tract. Both elements interact, and Ca supplements inhibit short-term iron absorption. However, studies are
lacking for longitudinal effect of short-term calcium supplementation on OS markers in healthy previously unsupplemented
women, relative to their blood calcium and iron panels. Present study assessed effect of short-term (30 days),
high-dose (1000 mg/day) calcium supplementation to 25 unsupplemented premenopausal women on Malondialdehyde
(MDA), superoxide dismutase (SOD), and circulating iron and calcium panels. Circulating Phosphorus (P) (13.46%), hemoglobin
(Hb) (7.32%), hematocrit (Hct) (8.02%), plasma iron (PI) (7.65%), transferrin saturation (TS) (9.65%) decreased
consistently in majority of respondents and Ca (4.91%), Total-Iron-Binding-Capacity (TIBC) (2.26%), Unsaturated-
Iron-Binding-Capacity (UIBC) (7.48%), MDA (30.1%) and SOD (58.59%) increased. Short-term, high-dose calcium
supplementation perturbed the blood levels of Ca, P and Ca/P, without alteration beyond known homeostatic ranges.
These changes were accompanied by effects on Hb, Hct and iron panels. Increased TIBC and decreased TS indicated reduced
intestinal iron absorption, attributable to high local calcium. Rise in MDA indicated OS but antioxidant metallozyme
SOD also increased, indicating an adaptive response to ameliorate OS related damage.