title: Association of organochlorine pesticides with the mRNA expression of tumour necrosis factor-alpha (TNF-α) & cyclooxygenase-2 (COX-2) genes in idiopathic preterm birth.
abstract: OBJECTIVE
  Preterm birth (PTB) is an important cause of prenatal death, neonatal morbidity and mortality and adult illness. Increased inflammation occurs in normal parturition, and inflammatory cytokines and oxidative stress are found to be higher in PTB cases. The present study was planned to investigate the association of organochlorine pesticides (OCPs) with mRNA expression of inflammatory pathway genes such as tumour necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2) in preterm delivery (PTD) cases.
  
  
  METHODS
  Maternal blood samples of PTD (n=30) cases and equal number of term delivery (n=30) were collected at the time of labour. Women occupationally exposed to OCPs and other high risk factors such as anaemia, hypertension, bacterial vaginosis, renal and heart disease, diabetes, etc. were excluded. The OCP levels were estimated by gas chromatography, and mRNA expressions of TNF-α and COX-2 genes were analysed using real-time PCR (qPCR).
  
  
  RESULTS
  Significantly higher levels of β-HCH (beta-hexachlorocyclohexane, 95% CI=2.08-4.633, p0 =0.001), p'p'-DDE (para, para-dichlorodiphenyldichloroethylene, 95% CI=0.546-2.551, p0 =0.003), and o'p'-DDD (ortho, para-dichlorodiphenyldichloroethane, 95% CI=0.004-0.690, P=0.047) were observed in maternal blood of PTB cases as compared to term delivery. The mRNA expressions of COX-2 and TNF-α genes were 3.13 and 2.31 folds higher in PTB cases in comparison to term delivery. l0 inear positive correlations were observed between period of gestation (POG) and ΔCt of COX-2 and TNF-α genes.
  
  
  CONCLUSIONS
  Environmental factors such as OCPs may be associated with inflammatory events showing gene-environment interaction in PTB cases. Evaluating the molecular control of inflammation along with gene environment interaction may be used as a model to explore the aetiology of idiopathic PTB cases and may be considered for the prognosis of adverse reproductive outcomes.
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: Vipin
authors.initials: V
authors.lastname: Tyagi
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: M D
authors.initials: MD
authors.lastname: Mustafa
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: Tusha
authors.initials: T
authors.lastname: Sharma
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: B D
authors.initials: BD
authors.lastname: Banerjee
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: Rafat S
authors.initials: RS
authors.lastname: Ahmed
authors.affiliation: Environmental Biochemistry & Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: A K
authors.initials: AK
authors.lastname: Tripathi
authors.affiliation: Department of Obstetrics & Gynaecology, University College of Medical Sciences & G.T.B. Hospital (University of Delhi), Delhi, India.
authors.forename: Kiran
authors.initials: K
authors.lastname: Guleria
mesh_terms: D000328:Adult; D051546:Cyclooxygenase 2 / Q000097:blood*; D004781:Environmental Exposure; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D059647:Gene-Environment Interaction; D006801:Humans; D006843:Hydrocarbons, Chlorinated / Q000633:toxicity; D007231:Infant, Newborn; D008297:Male; D018384:Oxidative Stress / Q000235:genetics; D010575:Pesticides / Q000633:toxicity*; D011247:Pregnancy; D047928:Premature Birth / Q000097:blood* / Q000139:chemically induced / Q000473:pathology; D012333:RNA, Messenger / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D006843:Hydrocarbons, Chlorinated; D010575:Pesticides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human