Cellular and subcellular antioxidants involved in liver susceptibility to xenobiotics.

Our previous studies have shown that some important serum erythrocyte and liver antioxidative defense factors--ceruloplasmine, catalase, superoxid dismutase, glutathione -SH and protein-SH groups--were sensitively affected by xenobiotics impact in rat. The data are completed here with the subcellular level of these factors. Dose or time exposure induced appreciable changes of the antioxidative factors (catalase, superoxid dismutase, ceruloplasmine) suggesting their redistribution between the subcellular fractions. The liver morphological investigations in all experimental variants express the aggressivity of Carbofuran administered alone and the "correctional" effects of the modulators' interference.

Interference of some enzymatic modulators in the hepatic aggression induced by xenobiotics.

The aim of the paper was to compare the erythrocyte serum and hepatic chomogenate antioxidative factors in order to assess their involvement in the detoxification events. The catalase and superoxiddismutase levels, important factors of the cellular defence, were sensitivity modulated in an acute experiment on Wistar rats. Carbofuran was administered in a non-lethal dose (7 mg/b.w.) single or in the presence of certain antioxidative agents (Vitamin E, Caffeine, Aspirin) EDTA and Cysteine for their role in protecting membranes against oxidative damage. The erythrocyte parameters (SOD, Catalase) were well related to seric factors, especially ceruloplasmin level, with varied magnitudes. GGT a marker of hepatotoxicity and G1-DH, a mitochondrial marker, were in a good correlation with erythrocyte factors. The changes seem to modulate a transmembranary disturbance process, as in hepatocyte pictures.

Simultaneous investigation of the rat serum and liver response in an acute toxic substances exposure.

Some biochemical parameters were simultaneously investigated in serum and hepatic homogenate in acute experiment with three pesticides in rat. The one-dose exposure response was relatively well correlated with the chemical toxicity and showed the statistically significant values, preferentially placed 48 hours after dosing. The liver morphological alteration might be associated with the serum and tissue comportment of the bioenzymological factors. The various genotoxicity induced by the three pesticides, appreciated by the frequency of micronucleus induction in the bone marrow cells, completes the data about the one-dose exposure effects of the chemical in rat.

Morphological and biochemical characteristics in the experimentally treated rats with indigenous synthetical products used as pesticides.

In acute experimental intoxication with 3 indigenous pesticides (Tripinacloraz, Lemax and Maleic Hydrazide-Na salt) the changes of some biochemical parameters, reflecting the degree of hepatic structural alterations, were studied. The pesticides were administered by gastric gavage in a single dose close to DL50 to Wistar male rats. The morphological alterations were in good correlation with a different hepatocellular levels localization. Reversible morphological lesions (granulovascuolar like dystrophy and circulatory disorders) without any pathological significance on dose-effect correlation induced a progressive response especially on serum ceruloplasmine, leucinaminopeptidase and lactatdehydrogenase.

Peripheral lymphocyte subpopulations changes during labor.

Peripheral circulating E-rosette-forming cells subpopulations (high affinity and low affinity E--RFC) were studied in pregnant women. In prelabor the high affinity/low affinity E--RFC ratio was found to decrease as compared with the controls by the decrease of the high affinity E--RFC (mean +/- SD, 33.4 +/- 15.9%, p less than 0.01) and the increase of the low affinity E--RFC percentage (mean +/- SD, 37.0 +/- 11.8%, p less than 0.001). As compared with prelabor the low affinity E--RFC subpopulation decreased during normal labor (mean +/- SD, 14.1 +/- 6.2%, p less than 0.001) and not in abnormal labor. These changes might be implicated in the final "fetal allograft rejection" and are probably due to some serum factors in pregnancy.