Role of complement and polymorphonuclear cells in demethylchlortetracycline-induced phototoxicity in guinea pigs. Inhibition by decomplementation in vivo.

Lim, Henry W.; Novotny, H.; Gigli, Irma

doi:10.1172/jci111088

Cited by 29 publications

(7 citation statements)

References 33 publications

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“…Chlorpromazine, hematoporphyrin, and demethylchlortetracycline are reported to become phototoxic products on UV irradiation (21,22,26,27). However, NA induces photohemolysis in vitro without becoming a toxic photoproduct conversion (14)(15)(16).…”

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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“…C5a has also been suggested to account for neutrophil-rich infiltrates observed at sites of tissue damage in the bullous eruption of systemic lupus erythematosus, dermatitis herpetiformis, bullous pemphigoid, and herpes gestationis (9,22,23). Recent studies have also shown that complement activation and generation of C5-derived chemotactic activity is relevant to lesion formation in patients with erythropoietic protoporphyria, porphyria cutanea tarda, and demethylchlortetracycline-induced phototoxicity (24,25).…”

Section: Skin Biopsiesmentioning

confidence: 99%

Studies of human C5a as a mediator of inflammation in normal human skin.

Yancey¹,

Hammer²,

Harvath³

et al. 1985

J. Clin. Invest.

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“…In guinea pigs, the clinical appearance of phototoxic lesions induced by demethychlortetracycline, a phototoxic agent, was markedly suppressed in animals that had been treated with cobra venom factor, an agent that resulted in 95% depletion of C3 activity and 60% depletion of C5 (18). These results were further corroborated by studies using the alteration in vascular permeability as the means to quantify the phototoxic response.…”

Section: Discussionmentioning

confidence: 74%

Activation of the complement system in patients with porphyrias after irradiation in vivo.

Lim¹,

Poh–Fitzpatrick²,

Gigli³

1984

J. Clin. Invest.

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A s bstract. Irradiation of the forearms of two patients with erythropoietic protoporphyria and one patient with porphyria cutanea tarda resulted in an in vivo activation of the complement system, as assessed by diminution of the hemolytic titers of the third component of complement by 23-57%, and of the fifth component of complement (C5) by 19-47%. Such treatment also generated chemotactic activity for human polymorphonuclear cells; the chemotactic activity was stable at 560C and antigenically related to human C5. On Sephadex G-75 chromatography the chemotactic activity eluted with an apparent molecular weight of 15,000. These in vivo results extend our previous in vitro observation of photoactivation of complement in sera from patients with erythropoietic protoporphyria and porphyria cutanea tarda, and suggest that the complement system may participate in the pathogenesis of cutaneous phototoxicity in these patients.

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Role of complement and polymorphonuclear cells in demethylchlortetracycline-induced phototoxicity in guinea pigs. Inhibition by decomplementation in vivo.

Cited by 29 publications

References 33 publications

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

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

Studies of human C5a as a mediator of inflammation in normal human skin.

Activation of the complement system in patients with porphyrias after irradiation in vivo.

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