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Biomedical subjects

L W Chang

Publications and source records attributed to L W Chang.

At least 91 records · Page 5Linked to original sources
PubMed1981

Binding of chemical carcinogens and mutagens to rat hemoglobin.

The alkylation of hemoglobin is a proposed dose monitor for chemical carcinogens and mutagens. The binding of fifteen chemical carcinogens and mutagens to rat hemoglobin was determined. Direct acting carcinogens and indirect acting carcinogens including aromatic amines, halogenated hydrocarbons, nitrosamines, polycyclic aromatic hydrocarbons, aflatoxin B1 and benzene bound hemoglobin. The efficiency of carcinogen and mutagen hemoglobin was dose dependent and ranged from 0.007 to 2.3% of an oral dose. The binding of chemical carcinogens and mutagens to hemoglobin would appear to be generic so that it could be developed into a dose monitor for a large number of known carcinogens and mutagens.

Animals↗
PubMed1980

An ultrastructural study on the reactive oligodendrocytes, myeloclasts, and myelophages in transected dog spinal cord.

As early as 1 to 3 hr after cord transection, proliferation of many reactive oligodendrocytes was observed. Bundles of microfilaments and microtubules were observed in those cells that sent out long, complex pseudopodlike processes near the area of injury. These reactive oligodendrocytes may be comparable to Vaughn's multipotential glia cells. Between 1 day and 1 wk, hypertrophy of the oligodendrocytes was observed. These hypertrophied oligodendrocytes also became hyperactive and infiltrated into the axons within the myelin sheath. These infiltrating hyperactive oligodendrocytes had a scanty fibrillary cytoplasm and are believed to correspond to Jakob's "myeloclasts". The infiltration of macrophages into the nerve fibers and myelin sheaths was also observed. These macrophages were found to be very active in phagocytosis and removal of degenerated debris within the nerve fiber and are believed to represent the "myelophages" described by Jakob in 1913.

Animals↗
PubMed1979

Cobalt-induced epilepsy: an ultrastructural study.

Metallic cobalt and aluminum rods were implanted into the cerebral cortices of rats. Almost all the animals with cobalt implantation were found to be epileptic 30 days after the operation. Tissue samples from the cerebral cortices were sampled for electron microscopy. The most significant changes in the cobalt-implanted animals were the disintegration of the rough endoplasmic reticulum in many cortical neurons and the accumulation of neurofilaments within the perikaryon. Such filamentous accumulation was usually found near the perinuclear position, at the periphery of the neurons, and in areas where there was a paucity of regular rough endoplasmic reticulum. Large aggregates of SER-like tubulovesicular structures were also found within many neuronal processes. Some of these neuronal processes could be identified to be postsynaptic dendritic terminals. Large nuclear pseudo-inclusions consisting of cytoplasmic materials were also found in some cortical neurons. These ultrastructural changes could also be occasionally observed in the opposite (cobalt-free) hemisphere of the brain (mirror image) in the cobalt-implanted animals. However, the brains of the aluminum-implanted or blank-control animals were free from any of these changes.

Aluminum↗
PubMed1978

Modification of methylmercury neurotoxicity by vitamin E.

The protective effect of vitamin E on the neurotoxicity of methylmercury was investigated by means of light and electron microscopy. Young male golden hamsters were exposed to 2.0 ppm methylmercury chloride with or without concurrent administration of vitamin E (2.0 ppm). No toxic symptoms were observed in the vitamin E-protected animals while all the animals given methylmercury alone developed severe symptoms of methylmercury poisoning. Light microscopy revealed no significant neural damage by mercury in those animals exposed to methylmercury/vitamin E while significant neuronal necrosis could be demonstrated in both the cerebellum and calcarine cortex of the methylmercury-treated animals. Besides some accumulation of lysosomes, electron microscopy also demonstrated remarkable intactness of the cellular organelles in the nerve cells without neuronal necrosis. It appears that vitamin E has a strong protective potential against the toxicity of methylmercury.

Animals↗
PubMed1978

Cadmium, a metallic inhibitor of antibody-mediated immunity in mice.

Chronic administration of cadmium chloride to B10-A-2R mice was discovered to severely depress the numbers and to delay the onset of appearance of splenic IgG and IgM plaque-forming cells (PFC) following injection of sheep erythrocytes. A recovery period of at least 1 month following cessation of administration of CdCl2 resulted in no increase in IgM PFC and only a minimal increase in IgG PFC. An apparent cadmium-induced splenomegaly was also noted in the intoxicated mice. Application of immune adherence and rosetting techniques as well as immunofluorescence to study the cellular morphology of these spleens indicated that the cell type most responsible for the increased spleen size had Fc and complement receptors as well as surface or cytoplasmic immunoglobulins. Populations of polymorphs and macrophages were not found to significantly contribute to the hyperplasia observed.

Animals↗