Preparation of rat liver plasma membranes in a high yield

Loten, Ernest G.; Redshaw-Loten, Jane C.

doi:10.1016/0003-2697(86)90512-9

Cited by 67 publications

(21 citation statements)

References 11 publications

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“…Crude and purified liver plasma membranes were prepared by modifications of published protocols (20,21). Briefly, crude membranes were obtained by homogenizing 0.5 g of liver in 0.25 M ice-cold sucrose at 20,000 rpm using an Ultra-Turrax homogenizer (IKA-LAB ortechnik, Staufen, Germany).…”

Section: Preparation Of Liver Membranesmentioning

confidence: 99%

Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia

Schaefer¹,

Chen²,

Tsao³

et al. 2001

J. Clin. Invest.

160

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Section: Preparation Of Liver Membranesmentioning

confidence: 99%

Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia

Schaefer¹,

Chen²,

Tsao³

et al. 2001

J. Clin. Invest.

160

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“…Rat gastric mucosa was totally excised and subcellular fractions were obtained as described in detail (Herná ndezMuñ oz and Montiel-Ruíz, 1996). Plasma membranes with a high level of purity were obtained by the method of Loten and Redshaw-Loten (1986). Cytosolic and microsomal fractions were also obtained by differential centrifugation, and the purity of the fractions was assessed with marker enzyme activities (Herná ndezMuñ oz and Montiel-Ruíz, 1996).…”

Section: Subcellular Fractionation Of Gastric Mucosamentioning

confidence: 99%

Gastric Mucosal Cell Proliferation in Ethanol-Induced Chronic Mucosal Injury Is Related to Oxidative Stress and Lipid Peroxidation in Rats

Hernández‐Muñoz

Montiel-Ruíz

Vázquez‐Martínez

2000

Laboratory Investigation

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SUMMARY:The oxygen free radicals-induced lipid peroxidation (LP) has been implicated in the pathogenesis of acute ethanol-induced gastric mucosal lesions. However, the role of LP in the generation of chronic gastric mucosal injury is unknown. We have developed a model of chronic mucosal injury induced by continuous ethanol ingestion for 5 days and characterized by marked alterations in plasma membranes from gastric mucosa. Therefore, LP was evaluated in this experimental model. Indicators of peroxidative activity, mucosal glutathione content, thymidine kinase activity (an index of cell proliferation), and histamine H 2 -receptor (H 2 R) binding constants were quantified in animals undergoing gastric mucosal damage. The effect of famotidine, a H 2 R antagonist that readily ameliorates the chronic mucosal injury, was also tested. Increased free radicals and LP levels were detected during gastritis; however, a second, higher peak of LP was noted in mucosal plasma membranes after ethanol withdrawal (recovery period). This further increase of LP coincided with active cell proliferation, decreased mucosal glutathione levels, and diminished specific cimetidine binding by H 2 R. Administration of famotidine accelerated the mucosal proliferative process, inducing the second lipoperoxidative episode sooner, and preserved the content of glutathione. In addition, LP correlated directly with cell proliferation and inversely with mucosal membrane cimetidine binding. In conclusion, LP seems to be involved in chronic ethanol-induced gastric mucosal injury. However, a further enhancement of plasma membrane LP occurred, associated with increased DNA synthesis and diminished cimetidine binding by membrane H 2 R. Therefore, increased LP could also participate in the compensatory mucosal proliferation initiated after ethanol withdrawal. (Lab Invest 2000, 80:1161-1169.

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“…Both and in five subcellular fractions obtained by differential cenmitochondrial and microsomal fractions were resuspended in the trifugation: mitochondria, cytosol, microsomes, plasma mem- procedures can affect basal liver LP, 10 the rate of LP proPlasma membrane fraction was obtained by centrifuging through moted by surgical removal of the liver was provided by coma Percoll gradient, as described by Loten and Redshaw-Loten. 12 Nuclei were prepared by the citric acid method reported by Reiners and parison of PH rats with proper sham controls ( Table 1). From Busch.…”

Section: In Addition Increased Lp Was Found In Microsomal Andmentioning

confidence: 99%

Selective Enhancement of Lipid Peroxidation in Plasma Membrane in Two Experimental Models of Liver Regeneration: Partial Hepatectomy and Acute Ccl4 Administration

1996

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with the rate of mitosis in several tissues, which has been It has been proposed that lipid peroxidation (LP) supported by the decreased LP found in subcellular fractions might be a modulator of cell division, influencing initiaof liver tumor cells. [2][3][4] However, some discrepancies have been tion and cessation of mitosis in regenerating liver. Howraised concerning the LP status during the characteristic acever, the understanding of the participating role of this tive cell proliferation following partial hepatectomy (PH). Acevent in the onset of liver proliferation has been hamtually, it was reported that both nicotinamide-adenine dinupered by the fact that both higher or lower LP have been cleotide phosphate-and tert-butyl hydroperoxide-induced reported after two-thirds partial hepatectomy (PH).LP were diminished after PH. [5][6][7] However, other research Therefore, the present study deals with the extent of LP groups have found an early increase of LP in homogenates in the main subcellular fractions from rat liver at early of regenerating liver. 8,9 Moreover, a transient enhancement stages of regeneration, induced by either PH of 70% or of mitochondrial LP has been reported to occur in preparaacute CCl 4 administration. Our results, using several tions obtained from hepatectomized rats. 10 methods to monitor LP, indicate a differential effect inThe present study was aimed at providing additional data the peroxidative pattern of specific subcellular fractions to settle the controversy about LP status during liver regenerfrom regenerating liver after 24 hours of PH: a decrease ation. We used two models to induce liver cell proliferation: in microsomes and an increase confined to plasma memtwo-thirds hepatectomy and acute intoxication with CCl 4 ; brane and cytosolic fractions, peaking after 24 hours of assessing LP by three different methods. The results show PH. In CCl 4 -treated rats, higher LP was also noted in that, in both models, an increased amount of LP activity is plasma membrane and cytosol, being maximal at the confined to the plasma membrane and cytosolic fractions, replicative stage in this experimental model (48 hours).whereas microsomes had a lower LP rate only in PH rats. In addition, increased LP was found in microsomal andThe changes in LP pattern, associated to liver regeneration, nuclear fractions, declining before the 48 hours. In hepashowed an organ specificity and correlated with the magnitectomized rats, changes in LP seem to be an organ-spetude of the loss of hepatic mass. The overall data suggest that cific event and related to only PHs capable of triggering controlled peroxidative modifications of membranes could be a synchronized proliferative response, namely above playing a role in the early steps of liver regeneration. fed ad libitum, and maintained under a 12-hour light/dark period. Surgical procedures were performed between 9 and 10 AM. Shamoperated animals were laparotomized under ether anesthesia to proThe liver is capable of recovering from damage or loss up vide a cont...

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Preparation of rat liver plasma membranes in a high yield

Cited by 67 publications

References 11 publications

Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia

Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia

Gastric Mucosal Cell Proliferation in Ethanol-Induced Chronic Mucosal Injury Is Related to Oxidative Stress and Lipid Peroxidation in Rats

Selective Enhancement of Lipid Peroxidation in Plasma Membrane in Two Experimental Models of Liver Regeneration: Partial Hepatectomy and Acute Ccl4 Administration

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