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Results for “Choline Deficiency”

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At least 1,315 records · Page 73Linked to original sources
PubMed2001

Adenoviral delivery of human and viral IL-10 in murine sepsis.

Adenovirus (Ad) gene therapy has been proposed as a drug-delivery system for the targeted administration of protein-based therapies, including growth factors and biological response modifiers. However, inflammation associated with Ad transduction has raised concern about its safety and efficacy in acute inflammatory diseases. In the present report, intratracheal and i.v. administration of a first-generation adenoviral recombinant (E1,E3 deleted) either containing an empty cassette or expressing the anti-inflammatory cytokines viral or human IL-10 (IL-10) was administered to mice subjected to zymosan-induced multisystem organ failure or to acute necrotizing pancreatitis. Pretreatment of mice with the intratracheal instillation of Ad expressing human IL-10 or viral IL-10 reduced weight loss, attenuated the proinflammatory cytokine response, and reduced mortality in the zymosan-induced model, whereas pretreatment with a control adenoviral recombinant did not significantly exacerbate the response. Pretreatment of mice with pancreatitis using adenoviral vectors expressing IL-10 significantly reduced the degree of pancreatic and liver injury and liver inflammation when administered systemically, but not intratracheally. We conclude that adenoviral vectors can be administered prophylactically in acute inflammatory syndromes, and expression of the anti-inflammatory protein IL-10 can be used to suppress the underlying inflammatory process.

Adenoviridae↗
PubMed1975

The role of endotoxin in liver injury.

Evidence is present that a common pathway for hepatic injury by a variety of agents may result from impairment of the liver's ability to detoxify bacterial endotoxins from the gastrointestinal tract. Many factors may structurally, metabolically, or hormonally alter the normal liver's ability to render innocuous the small amounts of lipopolysaccharide ordinarily presented to it. This impairment may accentuate existing hepatic damage by allowing toxic levels of endotoxin to develop in the liver tissue, and by allowing endotoxin entry into the systemic circulation, may also lead to extrahepatic effects. Studies are cited that: (1) support a role for intraintestinal endotoxin in the development of experimental cirrhosis. (2) demonstrate how liver injury alters endotoxin detoxification, (3) examine the role of intestinal production and absorption of bacterial lipopolysaccharides in liver disease, and (4) point to a role for endotoxemia in extrahepatic manifestations of liver injury as well. Studies are also reviewed that suggest possible mechanisms for modifying endotoxicity in hepatic damage.

Animals↗
PubMed1992

Orotic acid, nucleotide-pool imbalance, and liver-tumor promotion: a possible mechanism for the mitoinhibitory effects of orotic acid in isolated rat hepatocytes.

This study was designed to determine the possible mechanism by which orotic acid exerts its mitoinhibitory effect on rat hepatocytes in primary culture. Orotic acid inhibited, dose-dependently DNA synthesis in hepatocytes induced by epidermal growth factor, transforming growth factor alpha, hepatocyte growth factor, acidic fibroblast growth factor, or plasma from rats exposed to various liver cell-proliferative stimuli, such as two-thirds partial hepatectomy, lead nitrate, cyproterone acetate, ethylene dibromide, or a diet deficient in choline. Further, orotic acid inhibited DNA synthesis even when added 24 h after the hepatocytes were primed with transforming growth factor alpha. Taken together, these results suggested that the target site may not be at the level of the growth-factor receptor and receptor-mediated early events. In a preliminary experiment, orotic acid inhibited the expression of the ribonucleoside diphosphate reductase gene. Exposure to orotic acid results in an imbalance in nucleotide pools characterized by an increase in uridine nucleotides and a decrease in adenosine nucleotides. It is hypothesized that this imbalance in nucleotide pools inhibits the expression of the ribonucleoside diphosphate reductase gene and, therefore, is a likely target for the mitoinhibitory effect of orotic acid.

Animals↗
PubMedDate not supplied

[Effect of the reparative therapy on indices of lipid and phospholipid spectra of the blood plasma during neonathal enteropathology in calves].

The paper deals with dynamics peculiarities of quantitave changes of the same classes of lipid and phospholipid spectra of blood plasma of calves which have recovered from dyspepsia. The obtained reliable changes of blood plasma lipidogrammas testify to development of dyslipidhaemia, hypercholesterolhaemia and hyperthreacylglycerolhaemia as well as the deficiency of choline fractions of phosphatide--main structural components of cell membranes. It was established that changes of lipid and phospholipid spectrum of the blood plasma caused by enteropathology could be corrected by the inclusion of reparative therapy remedies to dyspepsia treatment plan, in particular, experimental phospholipids-containing remedy, which is prepared on the basis of milk phospholipids--their natural source for newborn calves.

Animals↗
PubMed1991

Light & electron microscopy of proliferating oval cells during early chemical hepatocarcinogenesis.

Early hepatic changes were studied in male albino rats (70) of Sprague Dawley strain fed a choline devoid diet containing 0.05 per cent w/w AAF (2-acetylaminofluorene) for 12 days. Proliferating periductal and ductal cells appeared in the portal area on days 1 and 3 respectively in the experimental group. On day 7, these cells infiltrated within the sinusoids of adjacent lobules up to the first one or two layers of hepatocytes. Subsequently, these cells extended up to the midzonal region on day 21 and by day 24 the entire lobule was infiltrated. Formation of duct like structures by the proliferating cells was seen on day 21. Ultrastructurally both periductal and ductal cells showed only a few organelles. Periductal and ductal cells are the earliest cells to appear in the portal area in chemically induced hepatocarcinogenesis. Its undifferentiated ultrastructure, may suggest the stem cell nature of these cells.

2-Acetylaminofluorene↗