phospholipidosis


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phospholipidosis

a generalized phospholipid disturbance with major deposits, derived from alveolar surfactant, in the pulmonary alveoli.
References in periodicals archive ?
2] results in unusual accumulation of non-degraded lung surfactant phospholipids in lysosomes of alveolar macrophages, leading to phospholipidosis, (80) perturbed presentation of endogenous lysophospholipid antigens to CD1d by invariant natural killer T (iNKT) cells, (81) and impairment of adaptive T cell immunity against mycobacterium.
In that study, an MDP approach was used and a subset of susceptible mouse strains sustained liver injury in response to the drug; mouse strains that experienced liver injury were subsequently found to exhibit phospholipidosis in Kupffer cells.
2003) Silymarin and vitamin E reduce amiodarone-induced lysosomal phospholipidosis in rats.
81 Oral bioavailability (VEBER) Good Phospholipidosis Non-inducer PPL_Friendly Yes Table 6 Molecular docking interaction of Glycosin with target receptors.
These alterations, the study reports, "were consistent with fibrosis, necrosis, phospholipidosis, mitochondria membrane dysfunction and ischemia.
Amiodarone-induced pulmonary toxicity (AIPT) is characterized in part by oedema, phospholipidosis, inflammation and thickening of the alveolar septa, intra-alveolar inflammation, and pulmonary fibrosis [3-5].
Lead-induced phospholipidosis and cholesterogenesis in rat tissues.
3 umol/l, it has been reported to cause moderate phospholipidosis with the characteristic changes of abnormal lysosomes containing electron-dense deposits and membranous structures arranged in whorled arrays (myelin figures) present in the cells21.
Gentamicin after removal from the serum is accumulated in renal tubular cells and produced phospholipidosis (Laureat et al.
Cytotoxic effects of oxysterols associated with human diseases: induction of cell death (apoptosis and/or oncosis), oxidative and inflammatory activities, and phospholipidosis.
After 13 weeks of dosing, multinucleated hepatocytes were reported for clarithromycin while Ketek elicited increased LFTs, increased NAGs (3x) in urine and phospholipidosis (FDA Briefing Package, 2001).
The initial underlying pathologic process in the lung from amiodarone toxicity is postulated to be a drug-induced phospholipidosis, (9) and the mechanism by which phospholipids accumulate in the cell is believed to be by inhibition of intracellular phospholipase when the drug and its metabolites are trapped in alveolar macrophages and type II pneumocyte lysosomes.