Carbon Monoxide and Avian Embryogenesis

Baker, Frederick D.; Tumasonis, Casimir F.

doi:10.1080/00039896.1972.10666050

Cited by 17 publications

(9 citation statements)

References 22 publications

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“…The high concentration of CO in tobacco smoke has led to the study of its effects upon embryonic development. It is noteworthy that a many studies in experimental models have reported some increase in developmental malformations resulting from CO exposure, including cleft palate and lip (Bailey et al, 1994), cardiac and respiratory defects (Potparic and Gibson, 1995), anencephaly (Daughtrey et al, 1983), eye and ear defects (Bnait and Seller, 1995), musculo‐skeletal defects (Baker and Tumasonis, 1972; McEwen, 1973; Loder et al, 2000) and other specific syndromes or defects (Potparic and Gibson, 1995; Schardein, 2000).…”

Section: Introductionmentioning

confidence: 99%

Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Alexander

Tuan

2003

Birth Defects Research

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We hypothesize that the somitic defects and the resulting axial skeletal dysmorphogenesis are caused by disrupted neural tube or ectoderm functions related to somite formation and maintenance. We also hypothesize that CO-induced dysmorphogenesis at this critical period of somitogenesis is caused by the overabundance of CO acting endogenously as a cellular signal, while coincidentally exerting its influence as a toxicant of oxygen delivery or utilization.

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Section: Introductionmentioning

confidence: 99%

Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Alexander

Tuan

2003

Birth Defects Research

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“…Another study demonstrated that maternal exposure to CO induced spinal deformities in mice [354]. Anencephaly [355], eye and ear defects [356] and skeletal abnormalities [357] associated with maternal CO exposure have also been reported.…”

Section: The Teratology Of Comentioning

confidence: 92%

Interactive Endogenous Small Molecule (Gaseous) Signaling: Implications for Teratogenesis

Fukuto¹,

Collins²

2007

CPD

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Dioxygen (O2) is an exogenously supplied gas with a number of properties that make it valuable as a biological source of energy and as a result much of life has become dependent on this molecule. Nitric oxide (NO), carbon dioxide (CO) and hydrogen sulfide (H2S) are small molecules that are sometimes in a gaseous state and that can be either exogenously or endogenously supplied. The chemistry of these four molecules allows them to share some common biological targets and signal transduction pathways as well as providing for unique aspects to the biochemistry of each one. Dioxygen can be teratogenic either in excess (hyperoxia) or in deficiency (hypoxia). Although there is a great deal known about the chemistry and physiology of dioxygen, the mechanisms by which it induces toxic endpoints, such as teratogenesis, are unknown. This review examines some fundamental concepts of these four signaling molecules and considers some of the molecular targets and pathways by which they interact. The information regarding the teratogenicity of either excess or deficiency of the four gases is summarized. Interaction information is generally unavailable for teratogenicity endpoints with the four gases and also a mechanistic understanding of the toxicodynamics of the compounds is lacking. Although it could be theoretically predicted that certain interactions would be additive, for example carbon monoxide and hypoxia, based on the physiological role of these molecules, the data is unavailable. Consequently, these small (gaseous) signaling molecules have been demonstrated to interact with respect to signaling pathways, but whether this indicates a similar result for teratogenesis remains unevaluated.

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“…There are few studies linking CO to congenital malformations in several animal models including chick, rabbit, and rat (Baker and Tumasonis, 1972; Murray et al, 1979); however, later studies failed to confirm this connection (Astrup et al, 1975). More recent studies exploring threshold levels and critical periods related to CO‐induced effects upon the embryo have documented CO‐induced dysmorphogenesis (Daughtrey et al, 1983; Bailey et al, 1995; Loder et al, 2000; Alexander and Tuan, 2003).…”

Section: Updates On the Teratogenic Mechanisms Of Selected Environmenmentioning

confidence: 99%

“…CO does impair oxygen delivery to and into cells by binding hemoglobin, myglobin, and other porphyrins; however, it may also function as a signaling molecule in the context of nitric oxide (NO) signaling (Maines, 1997). When administered after the vascular system is developed, the axial defects caused by CO are attributed to vascular leakage and subsequent mechanical disruption of developing tissue (Baker and Tumasonis, 1972). However, during early organogenesis, axial defects involve the reduction of important somite segmentation genes including PAX1 and Paraxis (Alexander and Tuan, 2003), resulting possibly in the impaired inductive interaction of the neural tube with the paraxial mesoderm with CO acting as a signaling molecule.…”

Section: Updates On the Teratogenic Mechanisms Of Selected Environmenmentioning

confidence: 99%

Role of environmental factors in axial skeletal dysmorphogenesis

Alexander¹,

Tuan²

2010

Birth Defects Research Pt C

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Approximately 1 in 1000 live births is afflicted with an axial skeletal defect. Although many of the known human teratogens can produce axial skeletal defects, the etiology of over half of the observed defects is unknown. The high morbidity associated with these defects demands that we continue to elucidate the mechanisms of axial skeletal teratogens. Advances in cell and molecular biology with respect to normal development and somitogenesis and the pathogenesis and mechanisms of teratogenesis are occurring at a tremendous rate. This allows teratologists and developmental toxicologists the opportunity to revisit old problems with new tools to elucidate common mechanisms between various environmental insults and discover novel targets that aid in the understanding of normal and pathogenic development of the spine.

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Carbon Monoxide and Avian Embryogenesis

Cited by 17 publications

References 22 publications

Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Interactive Endogenous Small Molecule (Gaseous) Signaling: Implications for Teratogenesis

Role of environmental factors in axial skeletal dysmorphogenesis

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