Role of oxidative stress while controlling iron deficiency anemia during pregnancy - Indian scenario

Iron Deficiency anemia ranks 9^th among 26 diseases with highest burden. Asia bears 71% of this global burden. Adverse maternal and birth outcome associated with hemoglobin status renders the issue worth attention. Indian scenario has worsened over the period despite continuous international and national efforts. This indicates some lacunae in the approach and strategies applied. Various reports state that even with maximum effort to increase outreach and monitoring for adherence to Iron schedule, consumer’s compliance remains abysmally low. Recent studies has pointed out biological basis of side effects (gastrointestinal complains and systemic events) as raised oxidative stress for which iron is the key catalyst. Up till now the only target of research has been to raise hemoglobin of pregnant women above 11gm/dl. With the reports of pregnancy specific morbidities i.e. hemorrhage and septicemia with low hemoglobin, eclampsia, small for gestation age, gestational diabetes with higher ranges of hemoglobin, alarm is raised to define optimum range. Use of oxidative stress as biochemical marker with different doses and schedules has been defined because India lack information for its own population upon oxidative stress status when iron is supplemented as per current guidelines. Studies done in India and abroad have defined that too much and too less, both may raise oxidative stress and studies of this sort may provide biochemical scale for optimization. This review therefore has evaluated currently available Indian research and reports to understand the need of future research area. Important findings from other countries have been incorporated for comparison.     

Comparative analysis of RBC membrane fatty acids, proteins and glycophorin in patients with heterozygous beta thalassemia and iron deficiency anemia

Membrane lipid and protein composition was compared in erythrocytes from iron deficiency anemia (IDA) and heterozygous beta thalassemia patients. The study was planned to correlate the influence of iron deficiency with the intrinsic defect of the heterozygous condition on the membrane structural integrity as well as to investigate whether there are differences in membrane changes between the two conditions. Results indicate high levels of saturated fatty acids and low unsaturated fatty acids in both disorders although arachidonic acid and the unsaturation index were lower in heterozygous thalassemia than IDA. Nevertheless, neither of the conditions provoked any alterations in membrane protein or glycophorin suggesting alterations in the lipid moiety only. Present findings indicate that irrespective to the etiology, both, iron deficiency and the heterozygous condition show a common pattern of lipid derangement, which may in turn result in increased membrane rigidity and decreased cellular deformability.     

Effect of iron deficiency on developing rat brain

Iron deficiency evolves, slowly through several stages. Early iron deficiency caused a depletion in iron stores as shown by a reduction in the levels of hepatic non heme iron (44%) in the 7 days old pups born to iron deficient mothers. The hemoglobin levels and PCV (packed cell volume) were significantly reduced only after the age of three weeks. The activities of GABA (γ-amino butyric acid) shunt enzymes viz. GDH, GAD and GABA-T (glutamate dehydrogenase, glutamate decarboxylase and GABA-transaminase, respectively) and GABA content were found to decrease during gestation and/or lactation iron deficiency at 1 week (wk), 2wk, 3wk and 4wk of age in the developing rat brains. However GABA binding showed a significant increase at different age groups. The iron deficiency during lactational exposure showed significant alteration in most of the parameters only at the age of 3 weeks onwards. On rehabilitation with iron supplemented diet for 2 weeks, these altered parameters could not attain corresponding control values. A prolonged iron deficiency causing alterations in GABA may lead to neurological and behavioral alterations.     

Comparative analysis of RBC membrane lipids in thalassemia, and iron deficiency anemia in relation to hypochromia and oxidant injury

The effect of an intrinsic defect in the red cell and pronounced hypochromia on oxidative damage to RBC membrane lipids was compared in beta-thalassemia and iron deficiency anemia (IDA), which have a varied etiology but equivalent low hemogiobin content. The study was planned to correlate the etiology of the disorders to the severity of lipid imbalance and RBC hemolysis in membranes of both the conditions. Results indicated a fall of lysophosphatidylcholine(LPC), phosphatidylethanolamine(PE) and the unsaturated to saturated fatty acid ratio in both conditions, while phosphatidylcholine(PC) increased only in thalassemia. However, irrespective of the disease, sphingomyelin(SM), total cholesterol and phospholipid levels elevated and the hydrogen peroxide stress test indicated increased susceptibility of both pathologic RBCs to peroxidation. Present findings indicate that IDA and thalassemla, allow for considerable amounts of oxidative damage to membrane lipids, irrespective of their etiologles, and thus point hypochromia as an important contributor for inducing lipid imbalance and RBC hemolysis.     

高校科技成果转化动力机制缺失及其对策

以武汉、上海地区6所高校的专任教师和科研管理部门负责人为调研对象,进行高校科技成果转化动力机制调研,从政策导向动力机制、市场驱动动力机制、人才激励动力机制三维度分析和论述高校科技成果转化动力机制缺失的主要表现及其原因,提出优化高校科技成果转化动力机制的对策与措施。