Liver injury in hypervitaminosis A: Evidence for activation of Kupffer cell function

Thesis/Dissertation · Fri Jan 01 00:00:00 EST 1988

OSTI ID:5401903

Sim, W L.W.

The most important and novel finding of this work was enhanced liver Kupffer cell phagocytic and metabolic function by hypervitaminosis A. An animal model of hypervitaminosis A was developed in male Sprague-Dawley rats gavaged with 250,000 I.U. retinol/kg body weight/day for 3 weeks. Presence of hypervitaminosis A was indicated by characteristic changes in the fur coat, presence of brittle bones and spontaneous fractures and a significant increase in plasma and liver concentrations of retinyl palmitate while retinol levels remained the same as in controls. Hypervitaminosis A did not cause severe liver abnormalities as reflected by normal plasma glutamate pyruvate transaminase activity and bilirubin. The main change was a marked increase in size of the fat or Vitamin A storing cells. Measurement of clearance from blood of indocyanine green and {sup 99m}Tc-disofenin indicated this hepatocyte function was normal. Kupffer cell phagocytic function was enhanced in hypervitaminosis A as determined by clearance from blood of {sup 99m}Tc-sulfur colloid. In vitro, there was also evidence that treatment with high doses of Vitamin A activated or enhanced Kupffer cell function. Kupffer cells from control and Vitamin A treated rats were isolated by enzymatic dispersion, purified by centrifugal elutriation, and placed in culture. Activation was indicated by (1) increased phagocytosis of {sup 51}Cr-labeled opsonized sheep red blood cells (2) enhanced release of superoxide anion and (3) enhanced production of tumor cytolytic factor by Kupffer cells from Vitamin A treated rats.

• Research Organization: Arizona Univ., Tucson, AZ (USA)
• OSTI ID: 5401903
• Resource Relation: Other Information: Thesis (Ph. D.)
• Country of Publication: United States
• Language: English

Related Subjects

59 BASIC BIOLOGICAL SCIENCES
LIVER
PATHOLOGICAL CHANGES
MACROPHAGES
BIOLOGICAL FUNCTIONS
METABOLIC DISEASES
PATHOGENESIS
VITAMIN A
BIOLOGICAL EFFECTS
AMINOTRANSFERASES
BILIRUBIN
BIOLOGICAL MODELS
BLOOD-PLASMA CLEARANCE
CHROMIUM 51
ISOMERIC NUCLEI
METABOLISM
PHAGOCYTOSIS
RATS
TECHNETIUM 99
TRACER TECHNIQUES
ANIMAL CELLS
ANIMALS
AZOLES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BODY
CARBOXYLIC ACIDS
CHROMIUM ISOTOPES
CLEARANCE
CONNECTIVE TISSUE CELLS
DIGESTIVE SYSTEM
DISEASES
ELECTRON CAPTURE RADIOISOTOPES
ENZYMES
EVEN-ODD NUCLEI
FUNCTIONS
GLANDS
HETEROCYCLIC ACIDS
HETEROCYCLIC COMPOUNDS
HOURS LIVING RADIOISOTOPES
INTERMEDIATE MASS NUCLEI
ISOMERIC TRANSITION ISOTOPES
ISOTOPE APPLICATIONS
ISOTOPES
MAMMALS
NITROGEN TRANSFERASES
NUCLEI
ODD-EVEN NUCLEI
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
ORGANS
PHAGOCYTES
PIGMENTS
PYRROLES
RADIOISOTOPES
RODENTS
SOMATIC CELLS
TECHNETIUM ISOTOPES
TRANSFERASES
VERTEBRATES
VITAMINS
YEARS LIVING RADIOISOTOPES
550901* - Pathology- Tracer Techniques