Intracytoplasmic type A particles from mammary tumours and leukaemias of strain ICRC mice.

The ovarian-hormone-induced leukaemias of strain ICRC mice, with an abundance of intracytoplasmic type A particles in primary as well as transplanted lesions, were used to study morphological, biophysical, immunological and structural characteristics of type A particles. Mammary tumours of strains ICRC and C3H(Jax) were also used as sources for type A particles. The purified virions banded at the density of 1.20 g/ml in 12--60% linear sucrose-density gradient when subjected to spinning at 113,000 g for 4 h. The SDS-polyacrylamide-gel electrophoresis of type A particles from mammary tumours and leukaemias reproducibly resolved at least 8 polypeptides, 2 of these 54,000 and 24,000 dalton proteins, showing variable expression. Type A particles and B particles, despite the fact that each had a distinct polypeptide pattern, showed common antigens with different electrophoretic mobilities. Proteins of 24,000, 18,000 and 12,000 daltons from B particles were found to be antigenically related to those from type A particles. The bioassay studies carried out with purified A particles showed that 2/7 males of strain ICRC and 1/6 females of strain DBA-MTI developed leukaemias, as against none in the controls, when inoculated between the ages of 1-7 days. Spleen tumour and cervical tumour were seen in one female each of strain DBA-MTI

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)

The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes in in vitro conditions. The activity of catalase (CAT), superoxide dismutase (SOD) and acetylcholinesterase (AChE), as well as the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) were measured in human erythrocytes exposed (in vitro) to clomazone at varying concentrations in the range of 0, 100, 250 and 500 µg/L for 1 h at 37 °C.TBARS levels were significantly higher in erythrocytes incubated with clomazone at 100, 250 and 500 µg/L. However, erythrocyte CAT and AChE activities were decreased at all concentrations tested. SOD activity was increased only at 100 µg/L of clomazone. GSH levels did not change with clomazone exposure. These results clearly showed clomazone to induce oxidative stress and AChE inhibition in human erythrocytes (in vitro). We, thus, suggest a possible role of ROS on toxicity mechanism induced by clomazone in humans

Destabilisation and subsequent lysis of human erythrocytes induced by Plasmodium falciparum haem products.

In falciparum malaria, both infected and uninfected red cells have structural and functional alterations. To investigate the mechanisms of these modifications, we studied the effects of two Plasmodium falciparum haem products (haematin and malaria pigment in the synthetic form beta-haematin) on isolated human red blood cells (RBCs) and purified RBC ghosts. A dose- and time-dependent incorporation of haematin into RBC ghosts and intact cells was observed, which was in proportion to the extent of haematin- induced haemolysis. RBCs pre-incubated with haematin were more sensitive to haemolysis induced by hypotonic shock, low pH, H2O2 or haematin itself. Haemolysis was not related to membrane lipid peroxidation and only partially to oxidation of protein sulphydryl groups and it could not be prevented by scavengers of lipid peroxidation or hydroperoxide groups. N-acetylcysteine partly protected the oxidation of SH groups and significantly reduced haemolysis. In contrast, beta-haematin was neither haemolytic nor oxidative towards protein sulphydryl groups. Beta-haematin did destabilise the RBC membrane, but to a lesser extent than haematin, inducing increased susceptibility to lysis caused by hypotonic medium, H2O2 or haematin. This study suggests that the destabilising effect of haematin and, to a much less extent, beta-haematin on the RBC membrane does not result from oxidative damage of membrane lipids but from direct binding or incorporation which may affect the reciprocal interactions between the membrane and cytoskeleton proteins. These changes could contribute to the reduced red cell deformability associated with severe malaria