Evaluation of oxidative stress among coronary diabetics patients.

OBJECTIVES: Determination of the superoxide dismutase (SOD), glutathione peroxidase (GPX) and the total antioxidant status (TAS) and evaluation of inflammation by the use of high sensitivity C reactive protein (hs-CRP) among Tunisian coronary diabetic patients. MATERIALS AND METHODS: We measured the erythrocyte GPX activity and the plasmatic TAS concentration by colorimetric methods, the apolipoproteins [ApoA1, ApoB], hs-CRP and the fibrinogen by immunonephelometry assays. RESULTS: TAS and GPX were significantly decreased among patients compared to the controls [TAS: 1,14 +/- 0,28 mmol/l vs 1,55 +/- 0,35 mmol/l, GPX: 59,32 +/- 10,72 U/gHb vs 149,19 +/- 30,95 U/gHb]. For the coronary diabetic patients, the TAS is correlated positively with hs-CRP [r= 0,01, p<10(-3)]. Pearson's correlation shows a significantly positive correlation between GPX and TAS among all patients. CONCLUSIONS: Determination of antioxidative defense markers contributes to understanding the effect of stress oxidative on the development, prevention and therapy of cardiovascular disease. (www.actabiomedica.it).

[Metachromatic leucodystrophy. Clinical, biological, and therapeutic aspects]. / La leucodystrophie métachromatique Aspects clinique, biologique et thérapeutique.

Scholz's disease or metachromatic leukodystrophy (MLD) is a lysosomal storage disease caused by a deficiency in arylsulfatase A (ARSA: EC 3.1.6.8). This enzyme is responsible for the degradation of sulfatides commonly called cerebroside-3-sulfate or 3-O-sulfogalactosylcéramide in galactocérébroside and sulfate. The success of hydrolysis of these sphingolipids by ARSA necessarily depends on the presence of saposine B forms a complex with the substrate. The pathological accumulation of sulfatides in the nervous system (myelin, neurons and glial cells) results most often neurological, mental retardation, nervous disorders, blindness. The metachromatic granules accumulated in the central nervous system and peripheral compounds are highly toxic. These are at high levels in the urine of patients affected by the MLD. Arylsulfatase A activity is collapsed in these patients. Unfortunately, the value of enzyme activity is not a predictor of clinical severity of the neuropathology. In contrast, the study of the gene that codes for the ARSA is seen as a way to diagnose the simplest and most reliable of the disease to avoid misdiagnosis due to the presence of pseudodeficit. The conventional therapeutic approaches are essentially symptomatic. They were made in order to restore the enzyme activity of arylsulfatase A and prevent the progression of the pathological accumulation of sulfatides and consequently reduce morbidity associated with MLD.