Search PubMed⌕ Search

Biomedical subjects

A Azzarone

Publications and source records attributed to A Azzarone.

26 records · Page 2Linked to original sources
PubMed1991

Relationship between plasma and hepatic cytosolic levels of ornithine decarboxylase (ODC) and thymidine kinase (TK) in 70% hepatectomized rats.

Ornithine decarboxylase (ODC) and thymidine kinase (TK) are enzymes important for DNA synthesis, a process that is critical for cell renewal and regeneration. As such, they already have been used as surrogate markers of regeneration in tissue. In the present study, the activity of these two enzymes in plasma of rats and regenerating hepatic tissue following a 70% hepatectomy were determined. The results demonstrate that the changes in these enzyme activities in plasma reflect the changes obtained in the liver tissue. Thus, blood levels of ODC and TK can be used as a less invasive and nondestructive means of monitoring the regenerative response of the liver and possibly other tissues.

Animals↗
PubMed1991

Screening for candidate hepatic growth factors by selective portal infusion after canine Eck's fistula.

Completely diverting portacaval shunt (Eck's fistula) in dogs causes hepatocyte atrophy, disruption of hepatocyte organelles, fatty infiltration and low-grade hyperplasia. The effect of hepatic growth regulatory substances on these changes was assessed by constantly infusing test substances for four postoperative days after Eck's fistula into the detached left protal vein above the shunt. The directly infused left lobes were compared histopathologically with the untreated right lobes. In what has been called an hepatotrophic effect, stimulatory substances prevented the atrophy and increased hepatocyte mitoses. Of the hormones tested, only insulin was strongly hepatotrophic; T3 had a minor effect, and glucagon, prolactin, angiotensin II, vasopressin, norepinephrine and estradiol were inert. Insulin-like growth factor, hepatic stimulatory substance, transforming growth factor-alpha and hepatocyte growth factor (also known as hematopoietin A) were powerfully hepatotrophic, but epidermal growth factor had a barely discernible effect. Transforming growth factor-beta was inhibitory, but tamoxifen, interleukin-1 and interleukin-2 had no effect. The hepatotrophic action of insulin was not altered when the insulin infusate was mixed with transforming growth factor-beta or tamoxifen. These experiments show the importance of in vivo in addition to in vitro testing of putative growth control factors. They illustrate how Eck's fistula model can be used to screen for such substances and possibly to help delineate their mechanisms of action.

Animals↗
PubMed1991

Cell regeneration in the pathobiology of liver carcinomas.

It is known that there is a close relationship between cirrhosis and liver cancer. The proliferative phenomena characterizing liver cirrhosis seem to be predisposing factors for carcinoma. In fact, they differ from the self-limiting proliferative phenomena occurring in normal liver regeneration because they are associated with: 1) an abnormal hormonal pattern; 2) an altered arrangement of hepatocytes and non-parenchymal cells within the lobule; 3) an altered production of growth factors able to modulate liver regeneration; and 4) an abnormal oncogene expression. Under such conditions many carcinogens, which require the target cell to be in a replicative phase, have the opportunity to act.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

Effect of epomediol on taurocholate uptake in hepatocytes isolated from normal rats or rats with ethinyloestradiol-induced cholestasis.

In this study the effect of epomediol (1,3,3-trimethyl-2-oxabicyclo 2.2.2 ocatan-6,7-endo, endo-diol) (Clesidren) on rat hepatocyte bile acid transport was evaluated using [3H]-taurocholate as a probe, in order to clarify the mechanism of action of this drug. To this purpose, primary cultures were prepared with hepatocytes obtained from normal rats (Group I), and rats receiving a 4-day treatment with either epomediol (100 mg/kg) (Group II), or ethinyloestradiol (5 mg/kg) (Group III), or ethinyloestradiol plus epomediol (5 mg and 100 mg/kg respectively) (Group IV) or vehicle DMSO 50 microliters/kg) (Group V). All hepatocytes were isolated 10 days after the end of treatment. Hepatocyte [3H]-taurocholate uptake was evaluated in vitro after 48 hr of incubation in the presence or absence of epomediol. In both cases no difference was found when evaluating the uptake of hepatocytes from Group I, II and V. In the absence of epomediol [3H]-taurocholate uptake in hepatocytes from rats of Group IV was significantly higher than that observed in hepatocytes from rats of Group III. On the other hand, the presence of epomediol did not influence [3H]-taurocholate uptake in hepatocytes from rats of Group III, which remained significantly lower compared to that of control hepatocytes (Group V). The protective effect obtained when administering epomediol simultaneously with ethinyloestradiol (Group IV) was not due to its ability to compete with ethynyloestradiol for the binding to oestrogen receptors. Our results indicate that epomediol is able to restore a normal hepatocyte bile acid uptake when given in vivo simultaneously with ethinyloestradiol but does not influence bile acid transport in cultured hepatocytes. Further studies are required to better define the choleretic activity of this drug.

Animals↗