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We hypothesized that this may be due to the toxic effect of carbon monoxide (<jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>) from tobacco, which has previously been described to damage mitochondria in non\u2010pregnant adult smokers. Maternal peripheral blood mononuclear cells (<jats:styled-content style=\"fixed-case\">PBMCs<\/jats:styled-content>), newborn cord blood mononuclear cells (<jats:styled-content style=\"fixed-case\">CBMCs<\/jats:styled-content>) and placenta were collected from 30 smoking pregnant women and their newborns and classified as moderate and severe smoking groups, and compared to a cohort of 21 non\u2010smoking controls. A biomarker for tobacco consumption (cotinine) was assessed by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content> (enzyme\u2010linked immunosorbent assay). The following parameters were measured in all tissues: mitochondrial chain complex <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content> [cytochrome <jats:italic>c<\/jats:italic> oxidase (COX)] activity by spectrophotometry, mitochondrial <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> levels by reverse transcription polymerase chain reaction, oxidative stress by spectrophotometric lipid peroxide quantification, mitochondrial mass through citrate synthase spectrophotometric activity and apoptosis by Western blot parallelly confirmed by <jats:styled-content style=\"fixed-case\">TUNEL<\/jats:styled-content> (terminal deoxynucleotidyl transferase dUTP nick end labelling) assay in placenta. Newborns from smoking pregnant women presented reduced birth weight by 10.75 percent. Materno\u2010fetal mitochondrial and apoptotic <jats:styled-content style=\"fixed-case\">PBMC<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CBMC<\/jats:styled-content> parameters showed altered and correlated values regarding <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content> activity, mitochondrial <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>, oxidative stress and apoptosis. Placenta partially compensated this dysfunction by increasing mitochondrial number; even so ratios of oxidative stress and apoptosis were increased. A <jats:styled-content style=\"fixed-case\">CO<\/jats:styled-content>\u2010induced mitotoxic and apoptotic fingerprint is present in smoking pregnant women and their newborn, with a lack of filtering effect from the placenta. Tobacco consumption correlated with a reduction in birth weight and mitochondrial and apoptotic impairment, suggesting that both could be the cause of the reduced birth weight in smoking pregnant women.<\/jats:p>","DOI":"10.1111\/adb.12183","type":"journal-article","created":{"date-parts":[[2014,9,3]],"date-time":"2014-09-03T09:35:37Z","timestamp":1409736937000},"page":"159-170","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Molecular basis of reduced birth weight in smoking pregnant women: mitochondrial dysfunction and apoptosis"],"prefix":"10.1111","volume":"21","author":[{"given":"Gl\u00f2ria","family":"Garrabou","sequence":"first","affiliation":[{"name":"Muscle Research and Mitochondrial Function Laboratory CELLEX\u2010 IDIBAPS Faculty of Medicine\u2010University of Barcelona Internal Medicine Department\u2010Hospital Clinic of Barcelona  Barcelona Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica 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