title: Modulation of cyclophosphamide-induced early lung injury by allicin.
abstract: BACKGROUND
  Cyclophosphamide (CP) causes lung injury in rats through its ability to generate free radicals with subsequent epithelial and endothelial cell damage.
  
  
  OBJECTIVE
  This study was conducted to assess whether allicin can ameliorate CP-induced early lung injury in rats.
  
  
  METHODS
  Male Sprague Dawely rats were divided into four groups. Group I was the control group. Group II received allicin (50 mg/kg/d, p.o.) for 14 consecutive days. Group III was injected once with CP (150 mg/kg, i.p.). Group IV received allicin for seven consecutive days, before and after CP injection (150 mg/kg, i.p.). The parameters of study were serum biomarkers, lung tissue antioxidant profile and histopathological changes in lung tissue.
  
  
  RESULTS
  A single intraperitoneal injection of CP markedly altered the levels of several biomarkers in lung homogenates. Significant increases in lung content of lipid hydroperoxides were seen that paralleled the decreased levels of total reduced glutathione. Superoxide dismutase activity (SOD) was significantly increased. CP increased the level of serum biomarkers; total protein, lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-α). Pretreatment of rats daily with oral allicin seven days prior to and seven days after CP inject significantly inhibited the development of lung injury, prevented the alterations in lung and serum biomarkers associated with inflammatory reactions, with less lipid peroxidation (LP) and restoration of antioxidants. Moreover, allicin attenuated the secretion of proinflammatory cytokine, TNF-α expression in rat serum. In addition, allicin effectively blunted CP-induced histopathological changes in lung tissue.
  
  
  CONCLUSIONS
  Our results suggest that allicin is efficient in blunting CP-induced pulmonary damage.
authors.affiliation: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt.
authors.forename: Nora A
authors.initials: NA
authors.lastname: Ashry
authors.forename: Nariman M
authors.initials: NM
authors.lastname: Gameil
authors.forename: Ghada M
authors.initials: GM
authors.lastname: Suddek
mesh_terms: D000284:Administration, Oral; D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000633:toxicity*; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D003520:Cyclophosphamide / Q000633:toxicity*; D004220:Disulfides; D016166:Free Radical Scavengers / Q000008:administration & dosage / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D015227:Lipid Peroxidation / Q000187:drug effects; D055370:Lung Injury / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013441:Sulfinic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D018906:Antineoplastic Agents, Alkylating; D000975:Antioxidants; D015415:Biomarkers; D004220:Disulfides; D016166:Free Radical Scavengers; D013441:Sulfinic Acids; D014409:Tumor Necrosis Factor-alpha; C006452:allicin; D003520:Cyclophosphamide; D013482:Superoxide Dismutase