STUDY OF HEAT SHOCK PROTEINS IN THALASSAEMIC PATIENTS

When cells are exposed to a variety of stimuli, there is increased expression of stress or heat shock proteins, a major representative of which is hsp70. The objective of the present work was to investigate the endogenous expression of hsp70 in peripheral blood mononuclear cells and erythrocytes of patients suffering from b-thalassaemia and to correlate hsp70 levels with patients' antioxidant status. Blood samples were obtained from thalassaemia major patients aged 16-24 years. Hsp70 was identified with a mouse monoclonal anti-human hsp70 antibodies using the Western blot procedure. The total antioxidant status was determined by means of a commercial kit of RANDOX. It was established that: i) Hsp70 levels were low in mononuclear cells, ii) Hsp70 was not appreciably induced by incubation at 43°C, Hi) in erythrocytes, however, there was a marked endogenous expression ofhsp70 - thalassaemics express more hsp70 than control subjects, iv) the antioxidant status of thalassaemics was by about 20 % less than the control one. The increased endogenous hsp70 in thalassaemic erythrocytes was consistent with the hypothesis that the elevated levels of denaturated globins induced the expression of stress proteins during erythopoiesis. We are currently investigating whether there is a correlation between the severity of the clinical symptoms and hsp70 levels

Total antioxidant status and erythrocyte superoxide dismutase activity in patients with chronic hepatitis B and C

Damage of hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected hepatocytes is mediated by both a direct cytopathic effect of the viruses and by immunologic response of T-cells. However, other mechanisms such as oxidative stress, may also be involved in cellular damage. We conducted a study to investigate the status of superoxide dismutase activity (SOD) and the total antioxidant status (TAS) in a consecutive cohort of patients infected with HBV and HCV infections, including HBV patients in the chronic inactive state of the disease. The latter were included in an attempt to determine whether antioxidant status is affected even in cases where an obvious viral activity is absent. TAS and SOD were measured in 55 patients (43 HBV, 12 HCV) and 25 healthy controls. 17 out of 43 patients had chronic inactive HBV state, 15 had chronic hepatitis B and 11 had HBV-related cirrhosis. In the HCV group, 6 patients had chronic hepatitis C and 6 HCV-related cirrhosis. Erythrocyte SOD activity was determined in haemolysate from red blood cells using a kinetic spectrophotometer method. TAS was measured by a colorimetric assay. The mean TAS and SOD values in the total number of patients (1.20±0.12 mmol/L and 1040±255 U/g Hb, respectively) were significantly lower (p<0.001) compared to healthy controls (1.57±0.13 mmol/L and 1491±420 U/g Hb). Comparisons between groups showed significantly lower (p<0.001) TAS and SOD values in each subgroup of patients compared to healthy controls. A significant positive correlation was found between TAS and SOD in the total number of patients (n=55, p<0.01), in the chronic hepatitis group (n=21, p=0.01) and in the total group of HBV patients (n=43, p<0.01). We demonstrated a significant reduced antioxidant capacity in patients with chronic HBV and HCV as indicated by low TAS and SOD. These findings were independent of the virological, biochemical and clinical status of the patients, including those with chronic inactive HBV state. This could suggest that the tissue-related consequences of oxidative stress might start from the inactive stage of liver viral diseases. However, our observations should be viewed with caution and need to be tested in a larger numbers of patients in order to determine prospectively whether these findings have pathophysiological and/or clinical significance. Copyright © by BIOLIFE, s.a.s