[Meloxican-induced cholestasis].
The cholestasis by meloxicam has not been often described. However, we present here the clinic, laboratory, histologic and follow up of a patient with cholestatic hepatitis produced by this drug.
Aged↗
Biomedical subjects
A Cravero
Publications and source records attributed to A Cravero.
Regression of morphological alterations and oxidative stress-related parameters after acute lindane-induced hepatotoxicity in rats.
Changes in rat liver oxidative stress-related parameters, morphological alterations, as well as circulating and tissue levels of lindane were studied 1-7 days after the administration of a single dose of 60 mg of lindane/kg. One day after lindane treatment, a significant enhancement in the oxidative stress status of the liver was observed, characterized by an increase in thiobarbituric acid reactants production and in the microsomal generation of superoxide radical (O.-2) coupled to cytochrome P450 induction, and a decrement in the activity of superoxide dismutase (SOD) and catalase. Consequently, the O.-2 production/SOD activity ratio was enhanced two-fold. In this condition, light microscopy studies revealed the incidence of liver lesions in periportal areas, together with significant changes at the mitochondrial level observed by electron microscopy, which coincide with the maximal levels of lindane in the liver, adipose tissue, plasma and whole blood. Changes in oxidative stress-related parameters observed after 1 day of lindane treatment regressed to normal from the third day and thereafter, together with the decrement in circulating and tissue levels of the insecticide. It is concluded that morphological and oxidative stress-related changes induced in the liver by acute lindane intoxication are readily reversible, depend on the hepatic content of the insecticide, and seem to be conditioned by the changes in O.-2 generation.
Adipose Tissue↗
Liver necrosis induced by Wedelia glauca in rats. A light and electron microscopy study.
Clinical, pathological and ultrastructural changes in rats injected ip with extracts of Wedelia glauca are described. Macroscopic changes were congested livers with accentuated centrilobular vascular patterns. Microscopic hepatic lesions had variable degrees of degeneration and lytic necrosis of centrilobular hepatocytes. Ultrastructural liver changes were condensation of nuclear chromatin with loss of perinuclear membranes, enlargement of mitochondria with alteration of limiting membranes, disappearance of cristae and matrical rarefaction. The endoplasmic reticulum was dilated with detachment of ribosomes. Serum activities of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were increased.
Alanine Transaminase↗
Regulation of manganese superoxide dismutase (MnSOD) in chronic experimental alcoholism: effects of vitamin E-supplemented and -deficient diets.
In order to investigate the pathogenic mechanism responsible for liver injury associated with chronic alcoholism, we studied the effects of different dietary vitamin E levels in chronically ethanol (EtOH)-fed rats on the activity and mRNA regulation of the manganese superoxide dismutase (MnSOD) enzyme. Evidence is accumulating that intermediates of oxygen reduction may in fact be associated with the development of alcoholic liver disease. Since low vitamin E liver content seems to potentiate EtOH-linked oxidative stress, we studied the effect of EtOH treatment in livers from rats fed a diet deficient or supplemented with vitamin E. Chronic EtOH feeding enhanced hepatic consumption of vitamin E in both groups of EtOH-treated animals, irrespectively of the vitamin E level of the basal diet and the effect was observed in both the microsomal and mitochondrial fractions. Both EtOH-fed groups exhibited increased MnSOD gene expression, while the enzyme activity was enhanced only in the vitamin E-deprived group of EtOH-treated animals. The significant increase in manganese liver content found only in this last group could explain the rise of enzyme activity. In fact, in the absence of a parallel increase of the prosthetic ion manganese, MnSOD mRNA induction was not accompanied by a higher enzymatic activity. These findings support the role of oxidative alteration in the EtOH-induced chronic hepatotoxicity in which MnSOD response might represent a primary defence mechanism against the damaging effect of oxygen radical species.
Alcoholism↗