Weekly iron folic acid supplementation plays differential role in maintaining iron markers level in non-anaemic and anaemic primigravida: A randomized controlled study

AbstractAnaemia during pregnancy is most commonly observed and highly prevalent in South-East Asia. Various effective programmes have been laid down for its management, mainly daily supplementation of iron folic acid (IFA) tablets. Following the same, standard obstetrical practice has included the IFA supplementation without requiring the determination of iron deficiency. In this study, a total of 120 primigravida (N=60; non-anaemic (Hb>11g/dl) and N=60 anaemic (Hb=8–11g/dl)) were selected among those attending the Antenatal Clinic in Department of Obstetrics and Gynaecology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India. They were supplemented with daily and weekly IFA tablets till 6weeks postpartum. Corresponding changes in haemoglobin level on advance of pregnancy, side effects and compliance associated with daily and weekly IFA supplementation and its associations with iron status markers were studied. The inflammatory markers were also estimated. The statistical significance level (p<0.05) between the groups were assessed by applying unpaired t-test using SPSS (version 16.0). The obtained results publicized the salutary role of daily IFA supplementation in improving the haemoglobin level and iron status markers in anaemic pregnant women though the levels could not reach up to the non-anaemic haemoglobin levels. However, weekly IFA supplementation seems to be a better approach in non-anaemic pregnant women where almost comparable results were obtained in terms of haematological parameters, gestation length and birth weight.ConclusionWeekly IFA supplementation found to be as effective as daily supplementation in iron sufficient non-anaemic pregnant women whereas anaemic pregnant women should be prescribed daily IFA supplementation irrespective of iron replete/deplete state

1H NMR-Based Metabolic Signatures in the Liver and Brain in a Rat Model of Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a debilitating neuropsychiatric complication associated with acute and chronic liver failure. It is characterized by diverse symptoms with variable severity that includes cognitive and motor deficits. The aim of the study is to assess metabolic alterations in the brain and liver using nuclear magnetic resonance (NMR) spectroscopy and subsequent multivariate analyses to characterize metabolic signatures associated with HE. HE was developed by bile duct ligation (BDL) that resulted in hepatic dysfunctions and cirrhosis as shown by liver function tests. Metabolic profiles from control and BDL rats indicated increased levels of lactate, branched-chain amino acids (BCAAs), glutamate, and choline in the liver, whereas levels of glucose, phenylalanine, and pyridoxine were decreased. In brain, the levels of lactate, acetate, succinate, citrate, and malate were increased, while glucose, creatine, isoleucine, leucine, and proline levels were decreased. Furthermore, neurotransmitters such as glutamate and GABA were increased, whereas choline and myo-inositol were decreased. The alterations in neurotransmitter levels resulted in cognitive and motor defects in BDL rats. A significant correlation was found among alterations in NAA/choline, choline/creatine, and NAA/creatine with behavioral deficits. Thus, the data suggests impairment in metabolic pathways such as the tricarboxylic acid (TCA) cycle, glycolysis, and ketogenesis in the liver and brain of animals with HE. The study highlights that metabolic signatures could be potential markers to monitor HE progression and to assess therapeutic interventions

Corrigendum: Topical Ophthalmic Formulation of Trichostatin A and SurR9-C84A for Quick Recovery Post-alkali Burn of Corneal Haze

Alkali burn injury is a true ocular emergency of the conjunctiva and cornea that requires immediate precision. Lack of an immediate therapy can lead to a substantial damage in the ocular surface and anterior segment further causing visual impairment and disfigurement. We explored the regenerative capability of dominant negative survivin protein (SurR9-C84A) and histone deacetylase inhibitor trichostatin-A (TSA) in vivo, in a rat alkali burn model. A topical insult in rat eyes with NaOH led to degradation of the conjunctival and corneal epithelium. The integrity of the conjunctival and corneal tissue was increased by TSA and SurR9-C84A by improving the clathrin and claudin expressions. Wound healing was initiated by an increase in TGF-beta-1 and, increased endogenous survivin which inhibited apoptosis post-TSA and SurR9-C84A treatments. Protein expressions of fibronectin and alpha-integrin 5 were found to increase promoting corneal integrity. The cytokine analysis confirmed increased expressions of IL-1beta, IL-6, IL-12, IL-13, IFN-gamma, TNF-alpha, GMCSF, Rantes, and MMP-2 in injured cornea, which were found to be significantly downregulated by the combined treatment of SurR9-C84A and TSA. The ocular and systemic pharmacokinetic (PK) parameters were measured post-topical ocular administration of TSA and SurR9-C84A. The SurR9-C84A and TSA sustained relatively longer in the cornea, conjunctiva, and aqueous humor than in the tear fluid and plasma. Our results confirmed that a combination of TSA with SurR9-C8A worked in synergy and showed a promising healing and anti-inflammatory effect in a very short time against alkali burn. Therefore, a combination of TSA and SurR9-C84A can fulfill the need for an immediate response to wound healing in alkali burnt cornea. We also synthesized ultra-small chitosan nanoparticles (USC-NPs) targeted with alpha-SMA antibodies that can be used for delivery of TSA and SurR9-C84A specifically to the ocular burn site

Hepatoprotective effects of Liv-52 on ethanol induced liver damage in rats

762-766The mechanism of protective effects of Liv-52, a multiherbal hepatoprotective drug, on ethanol induced hepatic damage has been investigated. The results indicate that Liv-52 treatment prevents ethanol induced increase in the activity or the enzyme γ-glutamyl transpeptidase. Concomitantly there was also a decrease in ethanol accentuated lipid peroxidation in liver following Liv-52 treatment. The activity of antioxidant enzymes; superoxide dismutase, glutathione peroxidase and the levels of glutathione were decreased following ethanol ingestion. Liv-52 treatment was found to have protective effects on the activity of superoxide dismutase and the levels of glutathione. The results obtained from the study indicate hepatoprotective nature of Liv-52 which might be attributed to its ability to inhibit lipid peroxidation

KD, Hepatoprotective effects of Liv-52 on ethanol-induced liver damage in rats

SUMMAR

Acephate induced oxidative damage in erythrocytes

963-966<span style="font-size: 14.5pt;mso-bidi-font-size:7.5pt;font-family:Fd220671-Identity-H;mso-bidi-font-family: Fd220671-Identity-H;color:black">The effect of oral administration of acephate (360 mg/kg body weight), for 15 days, daily, was investigated on the erythrocytes of male rats. Activities of acetyl cholinesterase and glucose-6-phosphate dehydrogenase decreased, while those of glutathione-s-transferase and glutathione reductase increased. Decreased glutathione content and increased lipid peroxidation suggest that there was increased oxidative stress in the erythrocytes of treated animals. Increased cholesterol/phospholipid ratio in the erythrocyte membranes and morphological changes in RBCs (scanning electron microscopy studies) were observed in acephate treated animals. The results clearly suggest that acephate induced oxidative stress in erythrocytes leads to morphological changes. </span

<i>In vitro </i>effects of organophosphate pesticides on rat erythrocytes

292-296In vitro effects of various organophosphate pesticides (dimethoate, chlorpyrifos, ethion and monocrotophos) were studied on hemolysis, K+ leakage and lipid peroxidation in rat erythrocytes. All the four pesticides increased hemolysis and K+ leakage from erythrocytes, that was concentration and time dependent. On the contrary, there was decrease in lipid peroxidation in erythrocyte membrane. Effect of pesticides on lipid peroxidation could be due to pesticide itself abstracting protons or interacting with free radicals rather than polyunsaturated fatty acids (PUFA), thereby protecting the latter against peroxidation

Erythrocyte antioxidant enzymes in toxicological evaluation of commonly used organophosphate pesticides

580-583Erythrocytes are excellent models for the study of interactions of xenobiotics with biomembranes. Present work is designed to study the in vitro effects of some organophosphates (ethion, chlorpyrifos, dimethoate and monocrotophos) on rat erythrocytes. Treatment of erythrocytes with organophosphates resulted in decreased erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) activity, whereas activities of glutathione-s-transferase (GST) and glutathione reductase (GR) were increased. Reduced Glutathione (GSH) content of RBCs was decreased after treatment with the pesticides. Increased activities of GST and GR were due to induction of natural defense mechanism of erythrocytes against the toxicity of the pesticides. Membrane bound enzymes like acetylcholinesterase (AChE), Na+-K+-ATPase and Ca2+-ATPase were also inhibited. Altered activities of these enzymes along with decreased GSH content indicate increased oxidative stress in erythrocytes after treatment with organophosphate

Hepatotoxic effects of tert-butyl hydroperoxide (t-BHP) and protection by antioxidants

728-731t-BHP induced oxidative stress and Ca2+ function impairment in fresh hepatocytes was studied in order to understand its role in cytotoxicity. Viability of hepatocytes by the release of lactate dehydrogenase and methyl thiazoletetrazolium reduction method alongwith malondialdehyde formation indicated oxidative stress in the hepatotoxic action of t -BHP