Variations of serum lipoproteins during cell proliferation induced by lead nitrate

Dessì, S.; Batetta, Barbara; Carrucciu, A.; Pulisci, D.; Laconi, Sergio; Fadda, Anna Maria; Anchisi, C.; Pani, P.

doi:10.1016/0014-4800(89)90010-5

Cited by 15 publications

(10 citation statements)

References 16 publications

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“…In all animal models, cholesterol synthesis and esterification as well as HDL-C were taken into account. We found an increase of cholesterol synthesis and esterification during liver regeneration following partial hepatectomy [66], in liver hyperplasia occurring after a single administration of lead nitrate [67,68], and in the liver of diabetic rats given insulin as well as in that of fasting rats [69,70]. In all these models, the peak of synthesis clearly preceded the maximum incorporation of labelled thymidine into DNA and accompanied all proliferative processes.…”

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confidence: 85%

Cholesterol metabolism during cell growth: Which role for the plasma membrane?

Batetta

Sanna

2006

Euro J Lipid Sci & Tech

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Parenchyma proliferation is accompanied by a peculiar modification of the cholesterol metabolism involving both the growing tissue and the plasma compartment. The increase of cholesterol synthesis and uptake has been largely described in the literature and mainly ascribed to the increased requirement of cholesterol for new membrane biogenesis. The dramatic reduction of cholesterol efflux, which probably contributes to the increase of cholesterol esterification and accumulation, has also been largely described, although, further to acting as a prompt pool for membrane biogenesis requirements, its significance and possible influence on cholesterol homeostasis during growth has been almost completely neglected. In this short review, the most widely known modifications and new insights into the cholesterol metabolism during the growth of normal and tumoral cells will be discussed. Particular attention will be paid to the most widely known modifications of cholesterol storage and efflux. The possible implication of proteins in membrane cholesterol translocation causing cholesterol to be directed towards the ER for esterification by ACAT rather than being released by the appropriate external acceptor, i.e. HDL, during proliferation will be discussed. Keywords:Membrane cholesterol, HDL-C, cell proliferation, signal transduction. Cholesterol metabolism in non-growing cellsWith the exception of specialised cells such as hepatocytes, the majority of resting cells synthesise cholesterol only virtually, with the minimal amounts of the required sterols being obtained by an external source (via lowdensity lipoprotein (LDL) receptor), intracellular cholesterol esterification and efflux also being absent, in accordance with the low membrane turnover present in this condition. Under normal conditions, intracellular cholesterol homeostasis utilises a complex network of reactions capable of providing an adequate supply of cholesterol while avoiding possible conditions of toxicity for the cells. In the majority of cells, the cholesterol supply is regulated by the balance between endogenous synthesis in the endoplasmic reticulum (ER), under the control of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCoA-R), and uptake of exogenous cholesterol, involving endocytosis of the LDL receptor (LDL-r) complex [1]. Toxic conditions produced by excess free cholesterol can be avoided in several ways: by down-regulating cholesterol synthesis and uptake, by promoting esterification by acyl-CoA:cholesterol acyltransferase (ACAT) in the ER [2], and/or by transport to the plasma membrane with subsequent delivery to an external acceptor, i.e. highdensity lipoproteins (HDL) [3].However, it is a well-established fact that a pool of cholesterol completes a cycle to the membrane and returns to the ER with a half-time of 40 min [4], and numerous studies have been undertaken to clarify the mechanisms and the proteins involved in the transport of such a highly hydrophobic lipid between the various intracellular compartments [5][6][7].With regard to cholester...

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confidence: 85%

Cholesterol metabolism during cell growth: Which role for the plasma membrane?

Batetta

Sanna

2006

Euro J Lipid Sci & Tech

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“…Previous studies by our laboratories Changes in lipid metabolism are a common feature during neoplastic growth, both in humans and in different experimental model systems (Clark and Crain, 1986;Dessi et al, 1986Dessi et al, , 1989Dessi et al, ,b, 1994. However, the mechanisms underlying these changes are stfill unclear and complicated by the fact that the metabolic alterations are species specific and dependent on the histological type or the degree of malignancy.…”

Section: Rc6mentioning

confidence: 95%

“…Nevertheless, a decrease in crculating HDL levels is found in virtually all neoplastic and inflammatory diseases studied in both rodents and humans (Dessi et al, 1986(Dessi et al, , 1989(Dessi et al, , 1991(Dessi et al, ,b, 1994Feingold et al, 1993) suggesting that the mechanisms underlying changes in total cholesterolaemia and triglycerilaemia are presumably different from those responsible for lowering HDL levels.…”

Section: Rc6mentioning

confidence: 99%

“…Cell proliferation, either normal or neoplastic, is commonly associated with altered cholesterol metabolism, and in particular with decreased plasma HDL-cholesterol levels (Dessi et al, 1986(Dessi et al, , 1989(Dessi et al, , 1992b. It has been proposed that this reduction results from a decrease in the release of cholesterol from proliferating cells to HDL (Daniels et al, 1987).…”

Section: Rc6mentioning

confidence: 99%

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Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)

Dessı̀

Batetta²,

Spano³

et al. 1995

Br J Cancer

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In the past few years a large body of evidence has been accumulated indicating a possible central role of choksterol in the pathobiology of cancer. Alterations in the synthesis, uptake and intracellular content of cholesterol have been observed in a variety of experimental tumour models as well as in different types of human neoplasms (Anderson et al., 1981;Coleman and Lavietes, 1981;Yachnin et al., 1983;Dessi et al., ,b, 1994.Choksterol perturbations also include change in lipoprotein profiles in plasma compartment. In particular, a definite decrease in high-density lipoprotein (HDL) klvels is a consistent finding in both experimental rat tumours and human neoplass (Dessi et at., 1991(Dessi et at., ,b, 1994 despite the differences reported to exist between lipoprotein metabolism in rodents and humans (Dietschy et al., 1993). In contrast, changes in other serm lipid parameters, such as total cholsterol and tnglyceride klvels, appear to vary and to be speces specific and dependent on the histological type or tumour grade (Dessi et al., 1991(Dessi et al., ,b, 1994. Therefore, it is possible that the mechanistic basis for the altered HDL levels is different from that responsible for the observed changes in other serum lipid parameters. Admittedly, HDLs play an important role in the transport of excess cholesterol from extrahepatic tisues to the liver for reutilisation or excretion into bile (reverse cholesterol transport). It is thus conceivable that the observed low levels of HDL-cholesterol may be related, at least in part, to a decrased choklsterol efflux to HDL as a consequence of increased utilisation and storage in actively proliferating tissues, such as neoplasms. However, since precursor prticles of HDL are thought to derive from lipolysis of triglyceride rich lipoproteins (Eisenberg, 1984) (Eisnberg, 1984), the possibility that low HDL cholesterol concentrations observed during tumour growth may be secondary to the decreased triglyceride clarance from plasna, as a result of LPL inhibition, must also be considered Tumour necrosis factor (rNF), a pleiotropic cytokine primarily produced by activated macrophages in response to invasve stimuli (Beutler and Cerami, 1988), has been frequently reported as beng responsible for changes in lipid metaboism which occur in association with infections and tumours in a wide variety of species, including humans and rats (Feingold et al., 1987(Feingold et al., , 1992 Harada et al., 1990). TNF might affect plasm cholesterol, triglyceride and lipoprotein levels by both inhibition of adipose LPL activity and/or stimulation of hepatic lipogenesis (Feingold et al., 1992(Feingold et al., , 1993 lipid metabolism in rats bearing ascites hepatoma Yoshida AH-130 has been previously investigated in our laboratories. This tumour causes in the host a rapid loss of body weight, associated with mared perturbations of both protein (Tessitore et al., 1987 and lipid metabolism . Increased synthesis and progressive accumulation of cholesterol were observed in AH-130 cells. During tumour gr...

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“…We and another group have previously observed that serum T-CHO levels rise approximately 50-70% in male SD and Wistar rats at 12-72 hr after LN-administration. 10,11,27) Therefore, WKY might be less sensitive to the effects of LN than SHRSP, SD and Wistar rats, and might have a genetic abnormality in some sort of cellular factor playing an important role in the generation of LN-induced hypercholesterolemia. In addition, considering the present results regarding the measurement of liver weights, it is considered that development of LN-induced hypercholesterolemia is not necessarily correlated with that of liver hyperplasia.…”

Section: Fig 1 Changes In the Liver Weights Of Wky And Shrsp After mentioning

confidence: 99%

Effects of Lead Nitrate on Liver Weight and Serum Total Cholesterol Amounts in Stroke-Prone Spontaneously Hypertensive and Wistar-Kyoto Rats

Nemoto

Yasuda

Hikida

et al. 2011

JOURNAL OF HEALTH SCIENCE

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The administration of inorganic lead (Pb) ion to rats is well known to induce liver hyperplasia with liver enlargement and hypercholesterolemia. In the present study, the sensitivities of stroke-prone spontaneously hypertensive rat (SHRSP) and its normotensive control strain, Wistar-Kyoto rat (WKY), to these effects of Pb ion were estimated. Lead nitrate (LN) dissolved in a distillated water for injection was administered to male SHRSP and WKY by a single intravenous injection at a dose of 100 µmol/kg body weight. In WKY, significant increases in the liver weight were observed at 24 and 48 hr after LNadministration, while in SHRSP, no such significant increases were observed up to 48 hr later. On the other hand, increased levels of serum total cholesterol after LN-administration were significantly higher in SHRSP than in WKY at each time, although the constitutive (control) level was the opposite. The present findings suggest that there is different susceptibility between SHRSP and WKY to LN-induced liver hyperplasia and hypercholesterolemia and further indicate that development of hypercholesterolemia is not necessarily correlated with that of liver hyperplasia.

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Variations of serum lipoproteins during cell proliferation induced by lead nitrate

Cited by 15 publications

References 16 publications

Cholesterol metabolism during cell growth: Which role for the plasma membrane?

Cholesterol metabolism during cell growth: Which role for the plasma membrane?

Perturbations of triglycerides but not of cholesterol metabolism are prevented by anti-tumour necrosis factor treatment in rats bearing an ascites hepatoma (Yoshida AH-130)

Effects of Lead Nitrate on Liver Weight and Serum Total Cholesterol Amounts in Stroke-Prone Spontaneously Hypertensive and Wistar-Kyoto Rats

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