Malondialdehyde, Antioxidant Enzymes, and Renal Tubular Functions in Children with Iron Deficiency or Iron-Deficiency Anemia

Demet Altun, Ahmet Emin Kurekci, Orhan Gursel, Duygu Ovunc Hacıhamdioglu, Ismail Kurt, Ahmet Aydın, Okan Ozcan

Araştırma sonucu: Dergi katkısıMakalebilirkişi

19 Alıntılar (Scopus)

Özet

We aimed to investigate the effects of iron deficiency (ID) or iron-deficiency anemia (IDA) on oxidative stress and renal tubular functions before and after treatment of children. A total of 30 children with a diagnosis of IDA constituted the IDA group and 32 children with a diagnosis of ID constituted the ID group. Control group consisted 38 age-matched children. Serum ferritin, soluble transferrin receptor (sTfR), serum, and urinary sodium (Na), potassium (K), calcium (Ca), phosphorus (P), creatinine (Cr), uric acid (UA), urinary N-acetyl-β-d-glucosaminidase (NAG) levels, and intra-erythrocyte malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were measured before and after iron therapy in the IDA and ID groups, whereas it was studied once in the control group. We have divided the study group in groups according to age (infants <2 years, children 3–9 years, and adolescents 10–15 years). Patients with IDA (infant, adolescent) and ID (infant, children, and adolescent) had a significantly high level of MDA in post-treatment period in comparison to those of healthy control. Patients with IDA (children, adolescent) and ID (infant, children) had a significantly high level of pre-treatment GSH-Px than controls. Post-treatment SOD was lower in IDA (children and adolescent) groups than control and post-treatment CAT was lower in IDA and ID (adolescent) groups than control. These findings show that ferrous sulfate used in the treatment of ID or IDA could lead to oxidative stress; however, a marked deterioration of in proximal renal tubular functions was not seen.

Orijinal dilİngilizce
Sayfa (başlangıç-bitiş)48-56
Sayfa sayısı9
DergiBiological Trace Element Research
Hacim161
Basın numarası1
DOI'lar
Yayın durumuYayınlanan - Eki 2014
Harici olarak yayınlandıEvet

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