Publication:
Melatonin reverses urinary system and aorta damage in the rat due to chronic nicotine administration

dc.contributor.authorŞENER, GÖKSEL
dc.contributor.authorELÇİOĞLU, HATİCE KÜBRA
dc.contributor.authorsSener, G; Kapucu, C; Paskaloglu, K; Ayanoglu-Dulger, G; Arbak, S; Ersoy, Y; Alican, I
dc.date.accessioned2022-03-12T17:16:23Z
dc.date.accessioned2026-01-11T15:24:45Z
dc.date.available2022-03-12T17:16:23Z
dc.date.issued2004
dc.description.abstractWe have evaluated the changes in contractile activity and oxidant damage of corpus cavernosum, urinary bladder, kidney and aorta after chronic nicotine administration in rats. The effects of melatonin on these parameters were investigated also. Male Wistar albino rats were injected intraperitoneally with nicotine hydrogen bitartrate (0.6 mg kg(-1) daily for 21 days) or saline. Melatonin (10 mg kg(-1), i.p.) was administered either alone or with nicotine injections. Corpus cavernosum, bladder and aorta were used for contractility studies, or stored with kidneys for the measurement of malondialdehyde and glutathione levels. Corpus cavernosum, bladder, and aorta samples were examined histologically and the extent of microscopic tissue damage was scored. In the nicotine-treated group, the contraction of corpus cavernosum, bladder and aorta samples and the relaxation of corporeal and aorta tissues decreased significantly compared with controls. However, melatonin treatment restored these responses. In the nicotine-treated group, there was a significant increase in the malondialdehyde levels of the corporeal tissue, bladder, kidney and aorta, with marked reductions in glutathione levels compared with controls. Melatonin treatment reversed these effects also. Melatonin administration to nicotine-treated animals caused a marked reduction in the microscopic damage of the tissues compared with those of the untreated group. In this study, nicotine-induced dysfunction of the corpus cavernosum, bladder and aorta of rats was reversed by melatonin treatment. Moreover, melatonin, as an antioxidant, abolished elevation in lipid peroxidation products, and reduction in the endogenous antioxidant glutathione, and protected the tissues from severe damage due to nicotine exposure.
dc.identifier.doi10.1211/0022357022818
dc.identifier.issn0022-3573
dc.identifier.pubmed15025861
dc.identifier.urihttps://hdl.handle.net/11424/227553
dc.identifier.wosWOS:000221770000010
dc.language.isoeng
dc.publisherROYAL PHARMACEUTICAL SOC GREAT BRITAIN
dc.relation.ispartofJOURNAL OF PHARMACY AND PHARMACOLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectDEPENDENT ARTERIOLAR DILATATION
dc.subjectSUPEROXIDE-DISMUTASE
dc.subjectLIPID-PEROXIDATION
dc.subjectNITRIC-OXIDE
dc.subjectENDOTHELIUM
dc.subjectREPERFUSION
dc.subjectISCHEMIA
dc.subjectSMOKING
dc.titleMelatonin reverses urinary system and aorta damage in the rat due to chronic nicotine administration
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage366
oaire.citation.issue3
oaire.citation.startPage359
oaire.citation.titleJOURNAL OF PHARMACY AND PHARMACOLOGY
oaire.citation.volume56

Files