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At least 433 records · Page 24Linked to original sources
PubMed1998

Antioxidant therapy of cobalt and vitamin E in hemosiderosis.

The protective effects of cobalt and vitamin E in iron overloaded rats were investigated. Rats were divided into four groups: group 1 as control, group 2 received only iron; group 3 iron and cobalt, group 4 iron and vitamin E. All injections were given 3 times per week for 3 weeks. Biochemical and histopathologic studies were done on samples of blood and liver, spleen, and intestine. The results showed that the administration of iron with cobalt or vitamin E decreased lipid peroxidation and the levels of hypoxanthine in all tissues (P < .001). Tissue associated myeloperoxidase (MPO) activity was increased in all iron-overloaded animals. However, vitamin E and cobalt decreased MPO activity (P < .001) in all tissues with the exception of the intestines, where cobalt was ineffective. Cobalt therapy increased hemoglobin, hematocrit, and MCV (P < .05). In contrast to SGPT activity, SGOT activity was significantly increased in all groups but more so in group 3 animals. The increased activity of serum SGOT levels might be related to the mechanical injury by cardiac puncture. The most striking histopathologic finding was the presence of granulomas in the livers of 71% of the animals of group 2 and in 66.6% of group 3. Interestingly, granulomas developed in only 33.3% of group 4 animals, whereas no granulomas were found in the livers of control animals (group 1). In this article we report that cobalt is as effective as vitamin E in significantly reducing iron-induced biochemical changes in an iron-overload in vivo model. We further describe for the first time the presence of extensive granuloma formation in iron-overloaded liver tissue and the greater efficiency of vitamin E over cobalt in protecting against granuloma formation in iron overload.

Alanine Transaminase↗
PubMed1999

Ferritin-associated iron induces neutrophil dysfunction in hemosiderosis.

Neutrophils (PMNs) from patients with secondary iron overload have an increased iron and ferritin content as well as a phagocytosis defect. Several serum components might be incriminated in the cellular iron accumulation. We therefore compared the effects on the PMN phagocytosis of total serum as well as the ferritin and transferrin fractions of serum derived from patients with thalassemia major and healthy control subjects. An incubation system of PMNs was developed. PMN phagocytosis was measured before and after incubation. Total serum from patients with thalassemia induced a defect that was prevented by co-incubation with deferoxamine (DFO). Gel-filtration chromatography was performed to separate the serum fraction containing transferrin and albumin from that containing ferritin. The transferrin-albumin fraction had no effect on PMN phagocytosis. On the contrary, the ferritin fraction of normal serum was deleterious to PMN phagocytosis, and the same fraction from thalassemic serum decreased PMN phagocytosis even more. Co-incubation with DFO or catalase improved this defect. Moreover, a cellular increase in the L-type subunit of ferritin was observed after the incubation of PMNs with the ferritin-containing fraction from thalassemic serum. In conclusion, serum from patients with thalassemia is toxic to PMNs, and this toxicity is due to ferritin-associated iron.

Adolescent↗
PubMed1998

Effects of experimental hemosiderosis on pancreatic tissue iron content and structure.

The effects of iron overload on pancreatic iron content and morphology were investigated. Sprague-Dawley rats were randomized into an iron-overloaded group, which received a single subcutaneous injection of 1.2 g/kg elemental iron as iron-dextran complex, and placebo-treated pair-fed controls. Animals were studied after a 10-month observation period. Tissue nonheme iron content was measured, and histologic examination was carried out. Chronic iron-overloaded animals showed significant increases in tissue iron content. There was a statistically significant increase in stainable iron in perivascular, parenchymal, and lymphoid tissue in the iron-overloaded group. Although pancreatic fibrosis was present in the iron-overload group, it was not statistically significant. The iron-overloaded animals showed some islet cell destruction. In contrast, no significant islet cell destruction was seen in the control group. However, the difference was not statistically significant. Moreover, the serum glucose levels were the same in both groups, suggesting that there was no significant impairment of pancreatic endocrine function. Thus, chronic experimental iron overload in rats leads to significant increases in tissue iron content, but no significant morphologic alterations of the pancreas with the dose and route of iron administered in this animal model.

Animals↗