Zinc Supplementation Attenuates Ethanol- and Acetaldehyde-induced Liver Stellate Cell Activation By Inhibiting Reactive Oxygen Species (ROS) Production and by Influencing Intracellular Signaling
Szuster-Ciesielska A; et al.
Biochem Pharmacol. 2009; 78(3):301-14.
(AA) Zinc has been reported to prevent and reverse liver fibrosis in vivo; however, the mechanisms of its action are poorly understood. We therefore aimed to determine the antifibrotic potential of zinc. Assessed was the influence of preincubation of rat HSCs with 30 microM ZnCl2 on ethanol- (in the presence of 4-methyl pyrazole (4-MP)) or acetaldehyde-induced toxicity, apoptosis, migration, expression of smooth muscle alpha-actin (alpha-SMA) and procollagen I, release of reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-alpha), tumor growth factor-beta1 (TGF-beta1), metalloproteinase-2 (MMP-2) and tissue inhibitors of metalloproteinases (TIMPs) production. Intracellular signals such as nuclear factor-kappaB (NFkappaB), C-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) induced by ethanol and its metabolite were also assessed. 30 microM zinc protected HSCs against ethanol and acetaldehyde toxicity and inhibited their apoptosis. Zinc inhibited the production of ROS by HSCs treated with ethanol and acetaldehyde and inhibited their migration. Zinc also inhibited ethanol- and acetaldehyde-induced TGF-beta1 and TNF-alpha production. Zinc down-regulated ethanol- and acetaldehyde-induced production of TIMP-1 and TIMP-2 and decreased the activity of MMP-2. In ethanol- and acetaldehyde-induced HSCs, zinc inhibited the activation of the p38 MAPK as well as the JNK transduction pathways and phosphorylation of IkappaB and Smad 3. The results indicated that zinc supplementation inhibited ethanol- and acetaldehyde-induced activation of HSCs on different levels, acting as an antioxidant and inhibitor of MAPK, TGF-beta and NFkappaB/IkappaB transduction signaling. The remarkable inhibition of several markers of HCS activation makes zinc a promising agent for antifibrotic combination therapies.
Compliance to Iron Supplementation During Pregnancy
Habib F, et al.
J Obstet Gynaecol, 2009 Aug; 29(6):487-92.
(AA) Iron deficiency anaemia is the most common nutritional disorder in the world. Pregnant women are at especially high risk of iron deficiency and anaemia because of significantly increased iron requirements during pregnancy. Iron supplementation during pregnancy has been recommended for women in the developing world, since usually no basic changes occur in the composition of the diet. This is a retrospective cohort study carried out in Al-Yamamah Hospital, Riyadh, Saudi Arabia, comparing the outcome of haemoglobin levels in 308 pregnant women near term with compliance to iron supplementation during the preceding pregnancy stages. Data were collected using an interview-based questionnaire for assessment of supplementation compliance and the women were divided into three categories: strictly compliant; partially compliant; and non-compliant. Haemoglobin levels were extracted from the medical records for the first antenatal visit (before 13 weeks' gestation) and compared with the level at entrance to the study at 36 weeks' gestation. Both Epi-info 2002 version 3.2 and SPSS version 10 were used for data analysis. Our results show that 49.7% used iron supplements continuously during the second and third trimesters of pregnancy; 38.3% reported partial use and 12.0% used no iron supplements. Haemoglobin levels improved significantly only among strictly compliant pregnant women, by 0.3 g/dl; decreased among partially compliant women by, 0.36 g/dl and significantly decreased among non-compliant, by -1.4 g/dl. Factors associated with non-compliance were education with a simple linear protective effect from being non-compliant. The percentage of anaemic women increased from 29.6% in the first trimester to 34% in the third trimester. Anaemia was significantly associated with non-compliance with iron supplementation, the adjusted OR was 6.19 95% CI 2.55-15.02, p <0.0001. Strategies to improve compliance and effective iron supplementation among pregnant women should be implemented.
Incidence of Anemia and Iron Deficiency in Strenuously Trained Adolescents: Results of a Longitudinal Follow-up Study.
Zhou Z, et al.
J Nutr Biochem; Aug 2009; 20(8):621-8.
(AA) Dietary copper (Cu) deficiency causes cardiac hypertrophy and its transition to heart failure in a mouse model. Cu repletion results in rapid regression of cardiac hypertrophy and prevention of heart failure. The present study was undertaken to understand dynamic changes of cardiomyocytes in the hypertrophic heart during the regression. Dams of FVB mice were fed a Cu-deficient (CuD) diet (0.3 mg Cu/kg) starting on Day 3 post-delivery, and weanling pups were fed the same diet until Cu repletion (6.0 mg Cu/kg) in the diet at 31 days of age. Heart samples were obtained at the end of CuD feeding or at 3, 7, 14 or 28 days after Cu repletion. Cu deficiency resulted in increases in the size and reduction in the number of cardiomyocytes in the heart. Cu repletion led to regression in the size of hypertrophic cardiomyocytes and normalization of the total number of cardiomyocytes. Although a direct reduction in the cell size would be significantly responsible for the regression of heart hypertrophy, some hypertrophic cardiomyocytes upon Cu repletion reentered the cell cycle as determined by Ki-67 staining in the cardiomyocyte-specific alpha-sarcomeric actin-stained cells and underwent division as determined by a mitosis-specific marker, phospho-histone 3. Quantitative analysis indicated that the replication of hypertrophic cardiomyocytes made a contribution of about one-third to the total mitosis of the regenerated myocardium. This study suggests that a direct reduction in the size of some hypertrophic cardiomyocytes and a replication of other hypertrophic cardiomyocytes with reduced size make a significant contribution to the regression of CuD heart hypertrophy, leading to normalization of the size and the number of cardiomyocytes in the heart.
Zinc Increases the Effects of Essential Amino Acids-Whey Protein Supplements in Frail Elderly
Rondondi A, et al.
J Nutr Health Aging; 2009; 13(6):491-7.
(AA) Protein undernutrition is frequent in the elderly. It contributes to the development of osteoporosis, possibly via lower IGF-I. Dietary zinc can influence IGF-I production. To determine the influence of dietary zinc addition on IGF-I and bone turnover responses to essential amino acids-whey (EAA-W) protein supplements in frail elderly. A daily oral protein supplement was given to hospitalized patients for 4 weeks. On a randomized, double-blind basis, patients received either an additional 30 mg/day of zinc or control. Sixty-one hospitalized elderly aged 66.7 to 105.8, with a mini-nutritional assessment score between 17 and 24 were enrolled. Activities of daily living; dietary intakes; serum IGF-I, IGF-BP3, CrossLapsTM, osteocalcin and zinc were measured before and after 1, 2 and 4 weeks of protein supplementation. Serum IGF-I rapidly increased in both groups. Zinc accelerated this increase with changes of +48.2 +/- 14.3 and +22.4 +/- 4.7% (p < .05) by 1 week, in the zinc-supplemented and control groups, respectively. Zinc significantly decreased the serum bone resorption marker CrossLapsTM by already 1 week. Activities of daily living improved by +27.0 +/- 3.1 and +18.3 +/- 4.5% in zinc-supplemented and control groups, respectively. In the elderly, zinc supplementation accelerated the serum IGF-I response to EAA-W protein by 1 week and decreased a biochemical marker of bone resorption.
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