PubMed · 7935694
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M J Smilkstein, D R Douglas, M R Daya. 1994-11-10. Acetaminophen poisoning and liver function.. https://pubmed.ncbi.nlm.nih.gov/7935694/
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The bulk crystallization of paracetamol has been examined under controlled conditions in the presence and absence of the additive p-acetoxyacetanilide (PAA), as a function of both supersaturation and additive levels. The induction time to nucleation was found to increase with increase in PAA concentration in solution. The product micro-crystals were characterized for shape and strain/defect content using electron and optical microscopy and X-ray Laue diffraction techniques, respectively. A change in crystal habit of the pure crystals from columnar (dominant [110]) to plate-like (dominant [001]) was observed to occur with an increase in supersaturation level, whilst the addition of PAA invariably led to the development of columnar crystals with an aspect ratio that varied with impurity level and supersaturation. HPLC showed the PAA to be incorporated into the crystals with an average segregation coefficient of 14-18% depending on the supersaturation. The ready incorporation of PAA is attributed to the molecular similarity of this molecule to that of the host material. The incorporation is shown to cause a significant increase in the mosaic spread, implying the development of a significant strain/defect content in the crystals. The influence of the impurity on the time to nucleation is probably due to its effect in blocking the development of the critical nucleus. The potential implications of such variations in morphology and strain content in the design of the physical and chemical properties of the resulting particulates are discussed.
Macrophages are critical cellular effectors of nonspecific host defense. They are also potent secretory cells releasing an array of mediators including proinflammatory and cytotoxic cytokines and growth factors, bioactive lipids, hydrolytic enzymes and reactive oxygen and nitrogen intermediates, each of which has been implicated in tissue injury. The research in our laboratories has focused on analyzing the role of macrophages in chemically induced injury in the lung and the liver. In both these tissues, a localized accumulation of macrophages is observed following toxicant exposure. This is directly correlated with the generation of cytotoxic inflammatory mediators at these sites. Moreover, when macrophage functioning is blocked, pulmonary and hepatic injury induced by toxicants such as ozone or acetaminophen is prevented. These findings provide direct support for our hypothesis that macrophages contribute to tissue injury. Approaches using pharmacologic inhibitors and transgenic animals are currently being used to evaluate the specific macrophage-derived products involved in the pathogenic process. Our results suggest that the extent to which a particular mediator contributes to injury depends on the nature of the toxicant, the target tissue, and quantities of the mediator produced.
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