The Effect of Substituted Naphthalenes on the Pilosebaceous Apparatus of Rabbit and Man1

Hambrick, George W.

doi:10.1038/jid.1957.11

Cited by 66 publications

(34 citation statements)

References 5 publications

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“…Hambrick 19 studied the histopathologic features of lesions of chloracne in different stages of evolution in human volunteers, and described that in early lesions of chloracne the epithelial cells of the outer root sheath forming the wall of the proximal portion of the infundibulum and the sebaceous duct appeared increased in number, resulting in dilatation of the proximal infundibulum. The walls of the sebaceous glands were thickened and merged with the infundibular wall.…”

Section: Histopathology Of Chloracnementioning

confidence: 99%

“…The maximum infundibular dilatation occurred proximally, resulting in either bottle-shaped formations, with the neck near the surface, or columnar funnels along the entire length of the infundibular structure. [19][20][21] Chloracne is easy to be diagnosed by history of exposure to chloracnegens, characteristic clinical manifestations and histopathology, and high serum concentration of chloracnegens. Chloracne has acneiform comedo and cyst, but different from acne vulgaris in etiology, pathogenesis, clinical features, histopathology and treatment (Table 1).…”

Section: Histopathology Of Chloracnementioning

confidence: 99%

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Environmental pollution and acne-chloracne

Qiang

Zouboulis

Xia

2009

Dermato-Endocrinology

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Environmental pollutants can result in a variant of acne called 'chloracne'. Chloracne is caused by systemic exposure to certain halogenated aromatic hydrocarbons 'chloracnegens', and is considered to be one of the most sensitive indicators of systemic poisoning by these compounds. Dioxin is the most potent environmental chloracnegen. Most cases of chloracne have resulted from occupational and non-occupational exposures, non-occupational chloracne mainly resulted from contaminated industrial wastes and contaminated food products. Non-inflammatory comedones and straw-colored cysts are the primary clinical manifestation of chloracne. Increasing of cysts in number is a signal of aggravation of chloracne. Generalized lesions can appear on the face, neck, trunk, exterimities, genitalia, axillary and other areas. Course of chloracne is chronic. Severity of chloracne is related to dosage of exposed chloracnegens, chloracnegenic potency and individual susceptibility. Histopathology of chloracne is characterized mainly by hyperplasia of epidermal cell, while follicular and sebaceous gland are taken placed by keratinized epidermal cell. The pathogenesis of chloracne maybe related to the imbalance of epidermal stem cell. Chloracne appears to be resistant to all tested forms of treatment. The only way to control chloracne is to prevent exposure to chloracnegens.

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Section: Histopathology Of Chloracnementioning

confidence: 99%

Section: Histopathology Of Chloracnementioning

confidence: 99%

Environmental pollution and acne-chloracne

Qiang

Zouboulis

Xia

2009

Dermato-Endocrinology

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“…Examples are chlorinated naphthalenes (Greenburg et al, 1939;Hambrick, 1957;Shelley and Kligman, 1957) and chlorinated phenols (Hofmann, 1957;Bauer e/ al., 1961;Bleiberg et al, 1964). The active compounds in chlorinated phenols have been identified as chlorinated dibenzodioxins (chlorinated diphenylene dioxides) which may appear as contaminants in the synthesis of chlorophenols (Bauer et al, 1961).…”

mentioning

confidence: 99%

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Vos

Beems

1971

Toxicology and Applied Pharmacology

115

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A significant difference in toxicity between 3 polychlorinated biphenyl (PCB) preparations was found in a prior study: Clophen A 60 and Phenoclor DP6 showing the highest, Aroclor 1260 the lowest, toxicity . A subsequent study revealed the presence of tetra-and pentachlorodibenzofuran in Phenoclor and Clophen . In the present study, application of 118 mg of the 3 PCB's (5 times per wk, for 38 days) on the back skin of rabbits also resulted in differences in toxicity.PCB-induced skin lesions were hyperplasia and hyperkeratosis of the epidermal and follicular epithelium. Histopathology of the liver included centrolobular degeneration, centrolobular liver cell atrophy, focal necrosis, and cytoplasmic hyalin degeneration. Definite hyperplasia and hyperkeratosis of the follicular epithelium of the ear skin were seen after the topical application of fractions of Phenoclor and Clophen eluted from chromatographic columns with 25 ",/, diethylether in hexane. The fraction from Aroclor caused a minimal hyperplasia and hyperkeratosis of the follicular epithelium. PCB-induced kidney lesions were hydropic degeneration of the convoluted tubules and tubular dilatation with the presence of casts. This dilatation was demonstrated also by a significantly increased relative percentage of the diameter which corresponds to the space of Bowman. Moreover, thymus atrophy and lymphopenia were found. Fecal coproporphyrin and protoporphyrin excretion was increased.

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“…The Halowax experiment. After time 2, a polychlorinated naphthalene compound and known comedogen (19), Halowax N-34 (obtained as a gift from Dr. Robert Cuozzo, Chemisphere Corp., Boonton, NJ), was applied to the human skin grafts in an attempt to produce follicular keratinization and microcomedo formation. An emulsion of mineral oil, acetone, and Halowax N-34 was prepared as described by Puhvel et al (20).…”

Section: Methodsmentioning

confidence: 99%

Development of a nude mouse model to study human sebaceous gland physiology and pathophysiology.

Petersen¹,

Zone

Krueger³

1984

J. Clin. Invest.

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Abstract. Study of human sebaceous gland physiology and pathophysiology is limited by lack of an adequate animal model. This study was designed to develop an animal model using human face skin grafted onto the nude mouse to study human sebaceous glands. Full-thickness human face skin was grafted onto 60 adult male nude mice. 4 wk after grafting, androgens, which are known to stimulate sebaceous glands, were administered to test the system. Androgens were administered to 21 animals by implanted catheters that were filled with testosterone (T) or dihydrotestosterone (DHT). Empty catheters were implanted in 15 control animals. Graft biopsies and blood for androgen levels were oW tained at time 1 (pre-catheter) and time 2 (26 d after catheter implantation). Three assessments were made on each biopsy: sebaceous gland volume, using an image analyzing computer; sebaceous cell size; and sebaceous gland labeling index. 29 mice completed the study through time 2. In the androgen-treated group, T levels (nanogram per milliliter) five times increased to 4.92±0.35, and DHT levels (nanogram per milliliter) increased 50 times to 16.70. In the androgen-treated group, sebaceous gland volume (,um3 X 10-3) increased from 896±194 to 3,233±754 (P < 0.001), sebaceous cell area (.um2) increased from 167±12 to 243±19 (P < 0.001), and labeling index (percentage) increased from 2.7±0.7 to 6.4±0.9 (P < 0.01). In the control group, sebaceous gland volume fell from 1,070±393 to 417±99

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The Effect of Substituted Naphthalenes on the Pilosebaceous Apparatus of Rabbit and Man1

Cited by 66 publications

References 5 publications

Environmental pollution and acne-chloracne

Environmental pollution and acne-chloracne

Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits

Development of a nude mouse model to study human sebaceous gland physiology and pathophysiology.

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