Oxidative stress in elderly chronic renal failure patients: effects of renal replacement therapies on cell membrane fluidity.

Background: Renal replacement therapies (RRTs) produce a partial loss of antioxidants and formation of reactive oxygen species (ROS), which are a major factor involved in alterations of plasma membrane fluidity and endothelial activation, but their role on plasma membrane fluidity in vivo is still unclear. We compared erythrocyte plasma membrane fluidity, ROS and total plasma antioxidant defenses (Lagtime) in aged patients with chronic renal failure (CRF) on conservative treatment, peritoneal dialysis (PD) and hemodialysis (HD) before (HD-pre) and after (HD-post) a treatment, to evaluate the role of different RRTs on oxidative stress and plasma membrane fluidity in aged patients.

Methods: We assessed erythrocyte plasma membrane fluidity, plasma lipid hydroperoxide levels and Lag-Time in 11 CRF patients on conservative treatment, 15 on PD, 12 on HD and 30 healthy controls.

Erythrocyte glycohydrolases in subjects with trisomy 21: could Down's syndrome be a model of accelerated ageing?

We studied some erythrocyte glycohydrolases, erythrocyte membrane fluidity, plasma hydroperoxides and total antioxidant defences in 23 Down syndrome (DS) individuals in comparison with healthy age-matched and elderly controls. With regard to erythrocyte plasma membrane fluidity, plasma hydroperoxides and total plasma oxidative defences, DS subjects resembled the age-matched controls more than the elderly ones. Membrane glycohydrolases in DS, however, presented a pattern partly similar to age-matched controls and partly to elderly controls.

Advanced oxidation protein products (AOPP) and high-sensitive C-reactive protein (hs-CRP) in an "atheroma-free model": Down's syndrome.

Murdoch et al. in 1977 called Down syndrome an "atheroma-free model." In this preliminary study, we investigated advanced oxidation protein products (AOPP) and high-sensitive C-reactive protein (hs-CRP) in 47 age-matched Down syndrome patients and 20 age-matched healthy controls.

Lysosomal leukocyte beta-D-glucuronidase during enzyme replacement therapy in Fabry disease.

Objective: Fabry disease results from a deficiency in the activity of alpha-d-galactosidase A and subsequent accumulation of neutral glycosphingolipids in lysosomes. This study investigated whether lysosomal enzymes can indicate biochemical changes in the lysosomal apparatus induced by enzyme replacement therapy (ERT).

Design And Methods: Eight patients were monitored by clinical and biochemical tests and several lysosomal glycohydrolases were measured in plasma and leucocytes.