Retinopathy from Inhaling 4,4′-Methylenedianiline Aerosols

Leong, B. K. J.; Lund, John E.; GROEHN, J. A.; Coombs, J. K.; Sabaitis, C. P.; Weaver, Royal J.; Griffin, Ronald C.

doi:10.1093/toxsci/9.4.645

Cited by 6 publications

(6 citation statements)

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“…Changes progressed thereafter to degeneration and thinning of the retina, including the photoreceptor segments, ONL and outer plexiform layer. POS destruction and accumulation of inclusion bodies in RPE cells have been described in the retinopathies induced by a variety of chemical agents: 2-aminooxy propionic acid derivatives, hexachlorophene, gentamicin, aminoglycoside antibiotics, netilmicin, cytosine arabinoside, phenothiazine derivatives, chloroquine, lead, laser, 2-phenyl-APB-144 (24), vitamin E deficiency (2), and 4,4'-methylenedianiline (25).…”

Section: Discussionmentioning

confidence: 99%

Phototoxic Lesions Induced by Quinolone Antibacterial Agents in Auricular Skin and Retina of Albino Mice

et al. 1993

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The phototoxic effects of quinolone antimicrobial agents on mouse auricular skin and retina were examined histologically. Sparfloxacin at 50 or 100 mg/kg, which alone causes no histologic change, was orally administered to albino Balb/c mice, which were irradiated with ultraviolet A for 4 hr immediately after administration. In the auricle, degeneration of basal epidermal cells was sporadically observed at 2 hr (during the irradiation). Foci of slight edema with degenerated fibroblasts were seen in the dermis at 4 hr. Edema and neutrophil infiltration in the dermis became severe up to 96 hr. Initial changes in the retina were observed at 2 hr. Vacuolation of the photoreceptor segments (particularly the inner segment) was occasionally associated with swelling of retinal pigment epithelial cells. The segments became disorganized with time, and the outer nuclear layer showed reduced cellularity. The segments and layer were partially thinned and lost 96 hr later. Enoxacin at 400 and 800 mg/kg induced similar lesions to those of sparfloxacin. Levofloxacin caused similar lesions in the auricle but no change in the retina. The combination of oral administration of quinolone and ultraviolet A irradiation, which never caused apparent morphological changes alone, was shown to be able to induce phototoxic lesions in albino mice. Therefore, this method is thought to be useful to examine morphological changes caused by quinolone phototoxicity.

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Section: Discussionmentioning

confidence: 99%

Phototoxic Lesions Induced by Quinolone Antibacterial Agents in Auricular Skin and Retina of Albino Mice

et al. 1993

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“…The chemical 4,4′-methylenedianiline is an intermediate in the production of isocyanates and polyurethanes. Inhalation causes degeneration of the photoreceptor inner and outer segments and degeneration of the RPE in both pigmented and unpigmented guinea pigs (Leong et al, 1987). Retinal degeneration has also been observed in cats poisoned via the peroral or percutaneous route (Schilling et al, 1966).…”

Section: Toxic Effects On the Pigment Epitheliummentioning

confidence: 99%

An Overview on the Toxic Morphological Changes in the Retinal Pigment Epithelium after Systemic Compound Administration

Mecklenburg

Schraermeyer

2007

Toxicol Pathol

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Many medications that are administered systemically for nonocular conditions may evoke ocular toxicological complications. Therefore, the eye is routinely investigated histopathologically in preclinical in vivo toxicity studies. The retinal pigment epithelium is a likely target for systemically administered compounds, since the underlying choroid is highly vascularized. The specialized pigment epithelium has numerous functions that all maintain the integrity and function of photoreceptors. Consequently, toxic effects on the pigment epithelium will eventually affect the neural retina. The potential of pigment epithelial cells to respond to toxic injury is limited, but a standardized terminology to describe its morphological changes does not exist in the scientific literature. Detailed morphologic analysis, however, might allow early detection of retinotoxicity and may provide evidence on the underlying pathomechanism. We here review toxic effects on the pigment epithelium focusing in particular on the morphology of toxic cell injury. Morphological changes comprise hypertrophy, intracytoplasmic accumulation of cellular components, loss of cell polarity, degeneration, metaplasia, and formation of subretinal membranes. Some of these changes are reversible whereas others are permanent, leading to impaired function of the pigment epithelium and eventually to photoreceptor loss and retinal atrophy.

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“…Carcinogenic compounds can cause irritation and inflammation at sites of exposure and are often antigenic (251)(252)(253)(254)(255)(256)(257)(258)(259). Respiratory carcinogens (or suspected carcinogens) include antimony compounds (260)(261)(262)(263), arsenic compounds (263)(264)(265)(266)(267)(268), hexamethylphosphoramide (269,270), 4,4´-methylene-bis(2-chloroaniline) (271,272), bromoform (273,274), methylene chloride (275), 4,4´-methylenedianiline (276,277), nitrobenzene (mice) (278-280), 4-nitrobiphenyl (281), 2-nitropropane (282)(283)(284)(285), N-nitroso-Nmethylurea (286), N-nitrosodimethylamine (287)(288)(289)(290), N-nitrosomorpholine (291-293), pentachlorophenol (mice) (294,295), polycyclic aromatic hydrocarbons (250,254,255), 1,3-propane sultone (296,297), propylene oxide (298-300), 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) (301-305), 2,4-toluene diamine (306,307), viny...…”

Section: Evaluating Human Exposure and Its Relationship To Asthmamentioning

confidence: 99%