Oxidative Stress in Families of Type 1 Diabetic Patients
Further evidence
- Elena Matteucci, MD and
- Ottavio Giampietro, MD
- From the Department of Internal Medicine, University of Pisa, Italy.
- Address correspondence to Prof. Ottavio Giampietro, Dipartimento di Medicina Interna (Clinica Medica II), via Roma 67, 56100 Pisa, Italy. E-mail: ematteuc{at}int.med.unipi.it .
We have recently reported evidence of increased oxidative stress in nondiabetic first-degree relatives of patients with type 1 diabetes (1). Elevated circulating markers of lipid peroxidation and increased cellular fragility seemed to be associated with supposed markers of inflammation. Transition metals may promote free radical reactions. Indeed, among radical-scavenging defenses of extracellular fluids, there are proteins involved in the sequestration of transition metals. Further-more it has been reported that cellular-redox modification influences the activity of ion-transport systems (2,3,4,5,6), including sodium/hydrogen exchange (NHE), and we have found increased erythrocyte NHE activity in families of patients with type 1 diabetes (7). Because we had previously examined the plasma thiol groups and the erythrocyte antioxidant reserves in type 1 families (8), we completed our investigation of possible first-chain initiating or stimulating factors.
In these families, we searched for the contribution of extracellular antioxidants to the increased levels of oxidative stress. We also investigated the eventual relationship between oxidative stress and abnormal NHE activity. The study groups were the same type 1 diabetic patients, first-degree relatives, and control subjects previously examined (1). We selected 30 type 1 diabetic patients (mean duration 20 ± 8 years; 10 without diabetic complications, 10 with retinopathy, and 10 with nephropathy and retinopathy), 36 nondiabetic normotensive siblings, 37 parents, and three groups of healthy subjects without …
