acid-phosphatase and dicarbine

The aim of the study is to perform a morphological analysis of certain lysosomal enzymes and parenchymal alterations during warm ischemia in the pig liver.. Standard hepatectomies were performed in a set of 24 pigs. Intra-operative intravenous (portal vein) Pentoxiphylline and hydroxyl radical scavenger Stobadine was administered. Tissue specimens were removed from the margo acutum in 10 minutes interval.. In normal pig liver, the acid phosphatase (ACP) activity is in not numerous Kupffer cells and on the biliary pole of hepatocytes, diffusely in the whole parenchyma. One hour after the beginning of warm ischemia, there was an increase in ACP activity in the cytoplasm of hepatocytes. The activity in Kupffer cells could not be detected. Lactate dehydrogenase (LDH) is localized exclusively in the cytoplasmic matrix of liver cells, so only cytoplasmic enzymes leak into the blood plasma. LDH activity has remained low in areas around portal and central veins.. Morphological findings of enzyme activities showed that zone 2 and 3 of the liver lobule are essential for the organ survival and signs of diffusion of lysosomal enzymes into the cytoplasm of hepatocytes indicate one of the possible explanations for the findings after liver reperfusion. The study showed that intravenous administration of Pentoxiphylline and Stobadine protects the liver from warm ischemia injury (Tab. 2, Fig. 2, Ref. 37). Full Text (Free, PDF) www.bmj.sk.

Topics: Acid Phosphatase; Animals; Carbolines; Free Radical Scavengers; Hepatocytes; In Vitro Techniques; Kupffer Cells; L-Lactate Dehydrogenase; Liver; Pentoxifylline; Swine; Warm Ischemia

This study investigated the ability of stobadine, an effective cardioprotective drug with antiarrhythmic, antihypoxic and oxygen free radical scavenging properties, to protect cells against cyclophosphamide-induced toxic and cytotoxic damage in vivo and in vitro. Cyclophosphamide-induced toxic damage in female ICR mice was accompanied by marked increase in the activity of lysosomal enzymes in the spleen and kidney. Administration of stobadine prior to cyclophosphamide inhibited these biochemical changes. The in vivo protective effect of stobadine was comparable with its in vitro effect established in HeLa cells.

Topics: Acetylglucosaminidase; Acid Phosphatase; Alkylating Agents; Animals; Antioxidants; Carbolines; Cyclophosphamide; Depression, Chemical; Female; Free Radical Scavengers; HeLa Cells; Humans; Liver; Lysosomes; Mice; Mice, Inbred ICR; Spleen

The antioxidant stobadine was tested for its efficiency against oxidative stress in model experiments with ICR nonpregnant mice exposed either to cyclophosphamide (80 mg/kg) or whole body 60Co (6.5 Gy) irradiation. In a teratological experiment, pregnant mice were exposed to cyclophosphamide (10 mg/kg) from day 11 to 17 of gestation. Toxicity was measured by determining the lysosomal enzymes acid phosphatase and N-acetyl-beta-D-glucosaminidase. Cyclophosphamide and irradiation caused a significant increase in acid phosphatase and N-acetyl-beta-D-glucosaminidase activity in the spleen of nonpregnant mice. In the liver, lysosomal enzyme activities were unchanged and no changes in protein levels were recorded. In pregnant mice, acid phosphatase and N-acetyl-beta-D-glucosaminidase activities were increased in the spleen. An increase in foetal acid phosphatase liver activity was found. Pretreatment with stobadine prior to cyclophosphamide and irradiation significantly diminished the biochemical changes in both nonpregnant and pregnant mice. We conclude that stobadine is able to protect mice against cyclophosphamide- or irradiation-induced oxidative stress.

Topics: Acetylglucosaminidase; Acid Phosphatase; Animals; Antioxidants; Carbolines; Cyclophosphamide; Female; Gamma Rays; Liver; Lysosomes; Mice; Mice, Inbred ICR; Oxidative Stress; Pregnancy; Spleen