title: Diallyl sulfide protects against ultraviolet B-induced skin cancers in SKH-1 hairless mouse: analysis of early molecular events in carcinogenesis.
abstract: BACKGROUND
  Diallyl sulfide (DAS) has been shown to have a preventive effect against various cancers.
  
  
  OBJECTIVE
  We evaluated the protective effects of DAS in regression of ultraviolet B (UVB)-induced skin tumor formation in SKH-1 hairless mice and its underlying early molecular biomarkers.
  
  
  METHODS
  We examined the efficacy of DAS in UVB light-induced skin lesion in SKH-1 hairless mice and the associated molecular events.
  
  
  RESULTS
  Mice irradiated with UVB at 180mJ/cm(2) twice per week elicited 100% tumor incidence at 20 weeks. The topical application of DAS before UVB irradiation caused a delay in tumor appearance, multiplicity, and size. The topical application of DAS before and immediately after a single UVB irradiation (180mJ/cm(2) ) resulted in a significant decrease in UVB-induced thymine dimer-positive cells, expression of proliferative cell nuclear antigen (PCNA), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and apoptotic sunburn cells, together with an increase in p53 and p21/Cip1-positive cell population in the epidermis. Simultaneously, DAS also significantly inhibited nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and nitric oxide (NO) levels.
  
  
  CONCLUSIONS
  The protective effect of DAS against photocarcinogenesis is accompanied by the down-regulation of cell-proliferative controls, involving thymine dimer, PCNA, apoptosis, transcription factors NF-κB, and of inflammatory responses involving COX-2, PGE2, and NO, and up-regulation of p53, p21/Cip1 to prevent DNA damage and facilitate DNA repair.
authors.affiliation: Department of Internal Medicine, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung, Taiwan, ROC.
authors.forename: Jaw-Ming
authors.initials: JM
authors.lastname: Cherng
authors.forename: Kuen-Daw
authors.initials: KD
authors.lastname: Tsai
authors.forename: Daw-Shyong
authors.initials: DS
authors.lastname: Perng
authors.forename: Jeng-Shing
authors.initials: JS
authors.lastname: Wang
authors.forename: Cheng-Chung
authors.initials: CC
authors.lastname: Wei
authors.forename: Jung-Chung
authors.initials: JC
authors.lastname: Lin
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology*; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004307:Dose-Response Relationship, Radiation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D051379:Mice; D008812:Mice, Hairless; D009363:Neoplasm Proteins / Q000096:biosynthesis; D009381:Neoplasms, Radiation-Induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012878:Skin Neoplasms / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013440:Sulfides / Q000494:pharmacology*; D013471:Sunburn / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D000498:Allyl Compounds; D016588:Anticarcinogenic Agents; D009363:Neoplasm Proteins; D013440:Sulfides; C038491:allyl sulfide