Oxidative criteria and somebone turnover markers in beta-thalassemic patients

Bone disease in beta-thalassemic patients has multifactorial etiology; increased iron stores and per-oxidative stress are involved factors. This study aimed to investigate the relationship between some bone turnover markers and some oxidants, antioxidants parameters of beta-thalassemic patients. The study included 50 patients were diagnosed as beta-thalassemia major aged between 3 and 40 years, 30 males and 20 females compared to 34 normal controls of same age and sex ratio. The patients and the controls were divided into 2 groups: group Al 18 years compared to their controls group B2. All were subjected to full clinical examination and laboratory analysis of their blood and urine for bone turnover markers; osteocalcin [OC], bone specific alkaline phosphatase [BAP] and urinary deoxypyridinoline [DPD].Also parathormone [PTH], serum calcium [Ca] and phosphorus [Ph]. Oxidants and antioxidants determined were; plasma malondialdehyde [MDA], nitric oxide [NO], blood reduced glutathione [GSH], erythrocyte Cu- Zn Superoxide dismutase [SOD]. Serum levels of copper [Cu], zinc [Zn], selenium [Se], vitamin E and total antioxidant capacity [TAOC] were also determined. The results showed significant increase in urinary DPD and decrease in serum OC, BAP and PTH in thalassemic groups compared to controls. Also, the results revealed significant elevation in plasma MDA, NO, SOD and serum Cu and TAOC especially in group Al. While there was significant decrease in GSH, serum Zn, Se, and vitamin E. Plasma OC was positively correlated with serum iron and NO and negatively correlated with plasma TAOC in thalassemic patients within age group 3

Iron status and lipid peroxidation in intermittent iron-supplemented rats

Despite extensive literature on iron and lipid peroxidation, few studies have investigated the effects of iron supplement on lipid peroxidation, The present study was designed to investigate the effect of intermittent iron supplementation on iron status, vitamin E status and lipid peroxidation in iron normal and iron deficient rats. Seventy two male Sprague-Dawley albino rats weighing [30-55 g] were divided into two groups [A and B], group A [32 rats] represents iron normal while group B [40 rats] represents iron deficient group. Group A was divided into 4 subgroups [1, 2, 3 and 4] and were fed on iron normal diet iron normal diet, with oral iron [l60mg/kg body weight] twice a week, iron normal diet with vitamin E supplementation [200mg/kg die] and iron normal diet with both oral iron dose and vitamin E supplementation respectively. Group B was divided into 5 subgroups, [I, II, III, IV and V] and were fed on iron normal diet, iron deficient diet, iron deficient diet with oral iron dose [160mg/kg body weight] twice a week, iron deficient diet with vitamin E supplementation [200mg/kg diet] and iron deficient diet with both oral iron dose and vitamin E supplementation respectively. Animals were fed ad libitum for 7 weeks. Blood hemoglobin [Hb], plasma iron, total iron binding capacity [TIBC], liver and kidney non heme iron, malondialdehyde [MDA] in [plasma, liver and kidney], blood glutathione [GSH], and vitamin E in [plasma and liver] were determined. The results showed that iron supplementation to normal rats led to a significant increase in blood hemoglobin, plasma iron, liver and kidney non heme iron, kidney MDA and slightly increase in plasma and liver MDA, while TIBC, plasma and liver vitamin E showed significant decrease. Iron supplementation to iron deficient rats led to markedly increase in blood Hb, plasma iron, liver and kidney non heme iron, blood GSH, liver and kidney MDA, while TIBC, plasma vitamin E showed a significant decrease. An improvement of iron status, lipid peroxidation, plasma and liver vitamin E levels were observed in groups which fed on diet contain vitamin E with or without oral dose of iron. In conclusion intermittent oral iron supplementation and daily supplementation of vitamin E could improve iron status and lipid peroxidation in iron normal and deficient rats

Ameliorative efficacy of a triple antioxidant combination of silymarin, selenium and vitamin E on thioacetamide induced liver cirrhosis in rats

This study was carried out to investigate the curative and protective efficacy of the triple antioxidant combination of silymarin, selenium [Se] and vitamin E [Vit.E] in thioacetamide-induced liver cirrhotic rats. Thioactamide [TAA] at a dose of 200 mg/kg, twice weekly, produced liver cirrhosis in rats as manifested by the significant [P<0.05] levation of hepatic marker enzymes and disturbances in antioxidant defense when compared with normal rats. Also, histopathologic evaluation of liver samples-demonstrated cirrhotic changes in TAA treated group. Oral administration of silymarin [20 mg/kg body weight], Se [10 micro mol/kg body weight] and vit. E in diet [1 g/kg diet] for 14 consecutive days, pre and post cirrhosis induction, significantly [P<0.05] decreased alanine and aspartate aminotransferase [ALT and AST, respectively], gamma-glutamyl transferase [GGT] and malondialdehyde [MDA] inthioacetamide treated rats. These ameliorative effects were more apparent in the post-treated group. The triple antioxidant also improved the activities of free radical detoxifying enzymes by increasing the activities of glutathione peroxidase [GSH-Px], glucose 6 phosphate dehydrogenase [G6P-DH], erythrocyte copper, zinc-superoxide dismutase [Cu, Zn-SOD] and the levels of reduced glutathione [GSH], plasma ceruloplasmin [Cp] and total protein in thioacetamide treated rats. A conclusion was made that the triple antioxidant induced marked improvement of biochemical and histopathological liver changes caused by thioactamide induction. Also, the results indicated that the potential therapeutic action of the triple antioxidant against TAA induction was more effective than its curative action

Exclusive breast feeding and nutritional status of infants

A longitudinal study was conducted to assess the nutritional status of 60 breast fed infants [37 females and 23 males] after delivery and up to the age of 6 months from different MCH Centers in rural areas. Weight, length an arm circumference were measured monthly as well as blood samples were collected to etermine hemoglobin and hematocrit. Wight-for-age, height-for-age, arm circumference for-age and incremental data for weight and length gains was used to determine nutritional status. Acute malnutrition tends to occur from about 2 months and 4 months of age among male and female infants respectively. Weight gains of female infants were greater than that of male infants. The sex related differences in length gain is manifested only at 2-4 months increments where it reached to 50 the percentile in male as compared to 5 the perecentile in female infants. Arm circumference-for-age revealed the presence of malnutrition among those infants irrespective of the sex. With the increase in age, the mean no. of epidoes of diarrhea and the average duration per individual per months were increased. Haemoglobin and hematocrit values showed a nor mal physiological pattern. So, growth failure of those infants may result from the prevalence of diarrhea among them as well as from a low quality of breast milk