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P Pani

Publications and source records attributed to P Pani.

At least 73 records · Page 4Linked to original sources
PubMed1987

Cell proliferation in rat kidney induced by 1,2-dibromoethane.

The effect of a single intragastric injection of 1,2-dibromoethane was investigated in kidneys of male Wistar rats. DNA synthesis as measured by the incorporation of tritiated thymidine was found to be approximately 5 times greater than that of controls 20-30 h after treatment. DNA synthesis was followed by a striking increase in the mitotic activity with a maximum at 30 h. The labeling and mitotic activities, after an initial increase, fell rapidly 48 h after treatment even though they were still higher than those of control animals. 1,2-Dibromoethane-induced cell proliferation is not a regenerative response because at the dose used in this study, no tubular necrosis was observed by histologic examination.

Animals↗
PubMed1987

Failure of mitogen-induced cell proliferation to achieve initiation of rat liver carcinogenesis.

Experiments were designed to determine whether mitogen-induced cell proliferation is as effective as regenerative cell proliferation in achieving initiation of liver carcinogenesis. To test this hypothesis male Wistar rats were injected with a single dose of diethylnitrosamine (DENA) or N-methyl-N-nitrosourea (MNU) during the peak of DNA synthesis following the administration of the liver mitogen, lead nitrate, after partial hepatectomy (PH) or a necrogenic dose of CCl4. The initiated hepatocytes were monitored as gamma-glutamyltransferase (GGT)-positive foci using a 2-week selection regimen consisting of 0.03% 2-acetylaminofluorene (2-AAF) coupled with a necrogenic dose of CCl4. The results indicate that unlike compensatory cell proliferation such as that induced by PH or CCl4, mitogen-induced cell proliferation did not result in any initiated hepatocytes despite the fact that in both types of models the extent of liver cell proliferation at the time of the administration of the carcinogen is similar.

Animals↗
PubMed1987

HMP-shunt and cholesterol metabolism in experimental models involving normal and preneoplastic liver growth.

Previous studies from our laboratories have shown a stimulation of HMP-shunt, cholesterol metabolism and DNA synthesis during cell proliferation. In order to understand the co-ordinated regulation of these pathways during cell growth, the above metabolic pathways were studied in: liver regeneration after partial hepatectomy, lead-induced liver hyperplasia, liver cell proliferation induced by insulin in streptozotocin-diabetic rats, liver cell proliferation in fasted rats after refeeding and, hepatocyte nodules induced by a selection procedure. The results indeed indicate that changes in HMP-shunt and cholesterol metabolism occur at a very early stage during the process of normal as well as preneoplastic cell growth. The coordinated regulation between cell growth and changes in these metabolic pathways needs further study.

Animals↗
PubMed1986

Hepatic glucose-6-phosphate dehydrogenase, cholesterogenesis, and serum lipoproteins in liver regeneration after partial hepatectomy.

Liver regeneration after partial hepatectomy was used as an experimental model for studying mammalian cell division and replication. The rate of cell proliferation in this hyperplastic model was correlated with hepatic de novo synthesis of cholesterol, with the hexose monophosphate shunt pathway of glucose metabolism, and with serum lipoproteins. An increase of hepatic cholesterol esters and of incorporation of tritiated water in cholesterol esters was observed at 24 hr after partial hepatectomy. Partial hepatectomy also resulted in an increase of hepatic glucose-6-phosphate dehydrogenase and in alteration of serum lipoproteins, primarily due to a selective decline in high density lipoprotein fraction.

Cholesterol↗
PubMed1986

Acinar cell carcinoma of rat pancreas: regulation of cholesterol esterification.

The regulation of cholesterol esterification during cell proliferation was studied. The serum free cholesterol, cholesterol esters and lecithin: cholesterol acyltransferase (LCAT) activity of nude mice with and without pancreatic acinar cell tumours and rats with proliferating tissues were determined. In addition, the apparent activity of acyl-CoA: cholesterol acyltransferase (ACAT) in homogenates of nude mouse tumours and proliferating rat tissues were determined and compared with those of normal nude mouse and rat tissues. Serum cholesterol ester levels were significantly lower in host nude mice with tumours and in rats with regenerating liver, and increased significantly in pregnant rats when compared with respective controls. Circulating LCAT activity levels decreased in host nude mice, in pregnant rats, and in rats with regenerating pancreas and regenerating liver. Apparent ACAT activity levels increased significantly in nude mouse tumours and in foetal and postnatal rat pancreata and also in postnatal liver. At the same time, apparent ACAT activity levels decreased in foetal and regenerating rat livers when compared with respective control tissues. These results suggest that serum cholesterol esters, circulating LCAT and cellular ACAT levels are modulated during cell proliferation.

Animals↗
PubMed1985

Hexose monophosphate shunt and cholesterol synthesis in the diabetic and fasting states.

The livers of streptozotocin-induced diabetic and fasted rats showed a decreased cholesterol synthesis measured by in vitro incorporation of [2-14C]acetate. A significant decrease of glucose-6-phosphate dehydrogenase (G-6-PD), 6-phosphogluconate dehydrogenase (6-PGD), and pyruvate kinase (PK) was also observed 7 days after administration of streptozotocin. These enzymatic activities were also low in livers of 72 hr fasted animals. An increase of glucose-6-phosphatase (G-6-Pase) was observed consistently in diabetic as well as in fasted rats. Suitable amounts of insulin and refeeding normalized the alterated enzymatic activities in diabetic and in fasted animals, respectively.

Animals↗
PubMed1985

Enhancement of cholesterol synthesis and pentose phosphate pathway activity in proliferating hepatocyte nodules.

The endogenous synthesis of cholesterol in hepatocyte nodules, induced in male Wistar rats, by a single dose of the hepatocarcinogen diethylnitrosamine followed by a selection procedure, was investigated and was compared with that in surrounding and control tissue. In addition, the activity of enzymes related to carbohydrate metabolism (glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glucose-6-phosphatase and pyruvate kinase), was measured. Hepatocyte nodules showed a striking increase in their capacity for synthesizing cholesterol, in comparison to surrounding and control tissues, and an enhancement in the activity of the pentose phosphate pathway, as indicated by increased activity of glucose-6-phosphate dehydrogenase and of 6-phosphogluconate dehydrogenase, and a concomitant decrease of glucose-6-phosphatase. The stimulation of cholesterol synthesis and of the pentose phosphate pathway was associated with increased incorporation of labelled thymidine into DNA. These data indicate that, among other metabolic disturbances, enhancement of cholesterol synthesis and of the pentose phosphate pathway, is accompanied by an increased proliferative capacity of hepatocyte nodules.

Animals↗
PubMed1985

Occurrence of cell death (apoptosis) during the involution of liver hyperplasia.

A single intravenous injection of lead nitrate at a dose of 10 mumoles/100 gm of body weight caused liver enlargement associated with hepatic cell proliferation. In the present study the involution of liver hyperplasia which follows the withdrawal of lead was studied in male Wistar rats. Histologic examination of liver sections from rats killed during the regression of the liver did not show any sign of massive lytic cell necrosis; no variation in the levels of serum glutamate pyruvate transaminase could be observed during the same time period; however, light microscopic observation of sections from the involuting liver showed the presence of several apoptotic bodies; the occurrence of apoptotic bodies was also confirmed by ultrastructural examination. Their incidence was found to be markedly increased at 5 days after treatment, a time period when the liver is already regressing; very few apoptotic bodies were observed in control animals or in treated rats 2 days after lead injection, a time point when mitotic index reached its maximum, or at 15 days, when the liver had returned to control values. These findings suggest that removal of excess liver which follows the initial hyperplasia caused by lead is due to a controlled mode of cell death, namely, apoptosis.

Alanine Transaminase↗
PubMed1984

Hepatic cholesterol in lead nitrate induced liver hyperplasia.

Wistar rats treated with lead nitrate were used in these experiments to provide evidence of the possible correlation between hyperplasia, induced cholesterol synthesis and the levels of glucose-6-phosphate dehydrogenase (G-6-PD) in the liver. Lead treatment increases liver weight, hepatic cholesterol esters and the relative content of free cholesterol. An increase of the incorporation of tritiated water in free and cholesterol esters was also observed. The effect of lead resulted in an increase of hepatic G-6-PD at all times considered. The correlation between these parameters and hyperplasia are discussed.

Animals↗
PubMed1984

Stimulation of DNA synthesis after a single administration of cadmium nitrate.

The effect of a single intravenous (i.v.) injection of cadmium nitrate was investigated in livers of male Wistar rats. A significant increase in liver weight, accompanied by an elevation of total hepatic DNA content was observed. DNA synthesis as measured by the incorporation of [3H]thymidine, was found to be 6 times greater than the control, at 24 h after treatment, and remained elevated over a period of 72 h. This elevation in DNA synthesis was not a consequence of cell necrosis, since no increase of serum glutamate-pyruvate transaminase (SGPT) activity was observed.

Alanine Transaminase↗
PubMed1984

Liver hyperplasia and regression after lead nitrate administration.

The effect of a single intravenous injection of lead nitrate on liver, was investigated in male Wistar rats. Lead nitrate at 5 and 10 mumoles/100 g of body weight stimulated a 19-fold increase in the incorporation of 3H-thymidine into liver DNA and resulted in temporal changes in DNA synthesis, as determined by assays of specific activity. Thirty-six hours after lead nitrate administration, the incorporation of 3H-thymidine reached its maximum and returned to normal levels within 3 days. A significant increase in the number of cells entering mitosis at 36 hours indicated the capacity of lead to stimulate liver cell proliferation. Enlargement of the liver after lead treatment was also observed in both female Wistar rats as well in male Fischer rats. This stimulatory effect of lead on liver growth was reversible; during the involution of the liver, cell death morphologically similar to the one described as apoptosis was observed in histological sections of liver from animals sacrificed 4-7 days after lead treatment.

Animals↗
PubMed1984

Changes in serum and hepatic cholesterol in lead-induced liver hyperplasia.

Lead nitrate when injected intravenously as a single dose to male Wistar rats causes a strong hepatic proliferative response followed by reabsorption of excess tissue within 10-14 days. The rate of cell proliferation in this hyperplastic model was positively correlated with hepatic de novo synthesis of cholesterol, stimulation of the hexose monophosphate shunt pathway of glucose metabolism and with alterations in serum lipoproteins.

Animals↗
PubMed1983

Effect of 3-MC on cholesterolemia and hepatic G-6-PD.

The effect of 3-methylcholanthrene (3-MC), an inducer of the mixed function oxidases system (MFOS), was investigated in male Wistar rats in relation to plasmatic cholesterol and hepatic glucose-6-phosphate dehydrogenase (G-6-PD). 3-MC induced an increase in total cholesterol; the maximal increase was seen 2 days after treatment (50%). The increase in total cholesterol was followed by an augmentation in cholesterol HDL. 3-MC treatment resulted also in an increase of hepatic G-6-PD.

Animals↗
PubMed1983

Lead and liver cell proliferation. Effect of repeated administrations.

The effect of repeated treatments with lead on hepatic cell proliferation was investigated in male Wistar rats. The animals were given intravenous injections of lead nitrate once every 10 days for 30 and 80 days. At the end of the experimental regimen, enlargement of the liver, accompanied by an increase in hepatic DNA content, was observed. A significant enhancement in the incorporation of labeled thymidine into hepatic DNA was found in lead-treated rats at the time intervals mentioned above, when compared with controls. An increase in the number of liver cells involved in mitosis was also observed in lead-treated animals. Analysis of serum glutamic-pyruvic transaminase and histologic observations did not show any sign of cell death at the time points examined. These results indicate that liver cells exposed to repeated treatments with lead undergo proliferation. However, a progressive reduction in the capacity of hepatic cells to divide was found in rats given repeated administrations of the metal, when compared with the extent of cell proliferation induced by a single dose of lead nitrate.

Alanine Transaminase↗
PubMed1983

Liver cell proliferation induced by a single dose of lead nitrate.

Treatment of male Wistar rats with a single dose of lead nitrate caused a marked enlargement of the liver, which reached its maximum 3 days after the administration of the metal salt. This grossly anatomic effect was accompanied by biochemical changes such as an increase in total protein and DNA content, with a maximum at 3 and 4 days, respectively. A partial regression of liver weight and total DNA and protein content occurred 7 days after lead administration; a significant increase in DNA concentration was found after 1 week, while no variation in protein, when expressed as milligrams per gram liver, was observed in lead-treated rat liver. An increase in DNA synthesis, as monitored by the incorporation of labeled thymidine, was also observed. An enhancement in the specific radioactivity of DNA was evident at 24 hours and appeared maximal at 36 hours after the administration of lead nitrate. The ability of lead to stimulate liver cell proliferation was shown by a significant increase of cells entering mitosis, with a peak at 48 hours. This mitogenic stimulus occurred in parenchymal as well as in nonparenchymal cells, thus showing that this effect was not unique to a particular liver cell populations. No detectable cell necrosis, as monitored by histologic observation, was seen in the liver of lead-treated rats, thus indicating that the cellular proliferation induced by lead is not due to a regenerative response. Only a slight elevation in the levels of serum glutamate-pyruvate transaminase (GPT) was observed by biochemical analysis.

Alanine Transaminase↗
PubMed1981

Cholesterol HDL in phenobarbital-treated male and female Wistar rats.

The effect of phenobarbital treatment on HDL cholesterol was studied in male and female Wister rats. An increase of HDL cholesterol was observed in both sexes one day after the administration of the barbiturate. The values of HDL cholesterol returned to those of the control animals l7 days after treatment.

Animals↗