Inhibition of n-hexadecane-induced epidermal hyperplasia due to systemically administered ciclosporin.
Epidermal hyperplasia was induced in hairless mice (hr/hr) by topical n-hexadecane treatment of tail and back skin. Following this skin irritation, a granular layer developed in interfollicular regions of the tail epidermis. An increase of ornithine decarboxylase activity, of thymidine triphosphate incorporation into DNA and of amino acid incorporation into protein was found. Shown histologically and by measurement of the called biochemical parameters, ciclosporin (cyclosporin A, CAS 59865-13-3; pretreatment with 30 mg/kg b.w. per day subcutaneously for 7 days) inhibited the development of epidermal hyperplasia in back and tail epidermis.
Lubach
D
D
Department of Dermatology (Hautklinik, Linden), School of Medicine, Hannover, Fed. Rep. of Germany.
Kietzmann
M
M
D000473:Alkanes / Q000037:antagonists & inhibitors* / Q000633:toxicity; D000818:Animals; D003524:Cyclosporins / Q000008:administration & dosage / Q000494:pharmacology*; D004247:DNA / Q000096:biosynthesis; D005260:Female; D006639:Histidine / Q000378:metabolism; D006965:Hyperplasia / Q000139:chemically induced* / Q000473:pathology; D007930:Leucine / Q000378:metabolism; D051379:Mice; D008812:Mice, Hairless; D065108:Ornithine Decarboxylase Inhibitors; D014176:Protein Biosynthesis; D012867:Skin / Q000473:pathology; D012871:Skin Diseases / Q000139:chemically induced* / Q000473:pathology; D013942:Thymine Nucleotides / Q000378:metabolism
D000473:Alkanes; D003524:Cyclosporins; D065108:Ornithine Decarboxylase Inhibitors; D013942:Thymine Nucleotides; D006639:Histidine; D004247:DNA; C007932:n-hexadecane; D007930:Leucine; C024157:thymidine 5'-triphosphate