Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Alexander, Peter G.; Tuan, Rocky S.

doi:10.1002/bdra.10041

Cited by 24 publications

(19 citation statements)

References 36 publications

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“…There is a known role for NO in bone [327]. These skeletal defects are comparable to the skeletal anomalies induced in chicken embryos following exposure to CO [328].…”

Section: B the Teratology Of Nomentioning

confidence: 73%

“…Additionally, many of the signaling pathways impacted by CO are oxygen-based signaling pathways [362]. However, a comparison of the CO-exposure phenotype with the hypoxia phenotype indicated differences between the two [328]. This suggested that CO disruption of organogenesis was mechanistically distinct from the hypoxic response.…”

Section: The Teratology Of Comentioning

confidence: 82%

“…Relatively recent experiments have demonstrated that CO exposure causes skeletal dysmorphogenesis in chick embryos and that this disruption of development resulted from the CO acting as an endogenous signaling molecule as well as acting as an inhibitor of oxygen delivery/utilization [328]. The role of CO as an endogenous signaling molecule during development is not well studied, however, animals that are null mutants for the two major isoforms of hemeoxygenase, HO-1 and HO-2, have been produced.…”

Section: The Teratology Of Comentioning

confidence: 98%

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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 is a known role for NO in bone [327]. These skeletal defects are comparable to the skeletal anomalies induced in chicken embryos following exposure to CO [328].…”

Section: B the Teratology Of Nomentioning

confidence: 73%

Section: The Teratology Of Comentioning

confidence: 82%

Section: The Teratology Of Comentioning

confidence: 98%

See 1 more Smart Citation

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

Fukuto¹,

Collins²

2007

CPD

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“…AVS is a common congenital abnormality that occurs with a prevalence of about 2-3/1000 births [24]. AVS can be divided into two main groups based on the number of vertebrae affected (Figure 2a).…”

Section: Abnormal Vertebral Segmentation In Humansmentioning

confidence: 99%

The role of Notch in patterning the human vertebral column

Dunwoodie

2009

Current Opinion in Genetics & Development

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“…Moreover, maternal smoking is the greatest identified cause of fetal weight deficiency, premature birth, miscarriage, perinatal/ neonatal death, neural tube defects, and congenital anomalies (6)(7)(8)(9)(10)(11). Furthermore, it adversely affects the development of organs and tissues serving several functions in cardiovascular and skeletal systems (12).…”

Section: Introductionmentioning

confidence: 99%

Ameliorating effects of curcumin on nicotine-induced mice testes

et al. 2016

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IntroductionTobacco addiction is the leading preventable cause of death, but the number of smokers is still rapidly increasing, particularly in undeveloped and developing countries (1,2).Cigarette smoking kills people by causing a wide range of diseases such as vascular disease and chronic lung disease. Principally, it increases the risk of mouth, oral cavity, pharynx, larynx, esophagus, pancreas, lung, cervix, bladder, and kidney cancers (2-5). Moreover, maternal smoking is the greatest identified cause of fetal weight deficiency, premature birth, miscarriage, perinatal/ neonatal death, neural tube defects, and congenital anomalies (6-11). Furthermore, it adversely affects the development of organs and tissues serving several functions in cardiovascular and skeletal systems (12).Nicotine is a major toxic component of cigarette smoke. Moreover, it is a strong alkaloid, which is isolated from tobacco leaves (13,14). It has been reported that nicotine passes through biological membranes, including the blood-brain barrier, and induces apoptosis and malformations (15). In addition to its pathogenic toxic effects on tissues and organs, nicotine has an impact on gonadal functions and inhibits ovulation, estradiol production, and fertilization (16)(17)(18). The production of free radicals (ROS), which impair the antioxidant system, is increased by nicotine (19,20). Therefore, an imbalance between ROS production and ROS elimination by the antioxidant system can cause oxidative stress in tissues (19)(20)(21)(22). As a cause of oxidative stress, it is well known that nicotine has detrimental effects on sperm count, motility, and morphology, and it impairs testicular structure and function, reducing the level of serum testosterone and estradiol (23-28). Antioxidant capacity against oxidative damage is extremely important for organs such as the testes, which have high metabolic activity and cell replication (29,30).Turmeric (Curcuma longa) is a perennial plant that has been used as a spice and medicine in Asian and African countries for thousands of years (31,32). Curcumin, which is obtained from turmeric roots, is used as an antiinflammatory, antiseptic, antioxidant, anticarcinogenic, and hypocholesterolemic agent in traditional medicine (33)(34)(35)(36). It is known that curcumin, Background/aim: The aim of this study was to determine the antioxidative effect of curcumin on nicotine-induced mice testis.Materials and methods: Sixty Swiss albino male mice were divided into five groups, each containing 12 mice. The first group was used as a control. To induce toxicity in the second and third group, nicotine (0.4 mg/kg/day) was injected intraperitoneally into mice for 14 and 28 days, respectively. The mice in the fourth and fifth group were injected with nicotine (0.4 mg/kg/day) and orally treated with curcumin (200 mg/kg) for 14 and 28 days, respectively. Testosterone levels were measured from blood samples and testis tissues were examined under light and electron microscopes.Results: Light and electron microscopic examinatio...

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Carbon monoxide‐induced axial skeletal dysmorphogenesis in the chick embryo

Cited by 24 publications

References 36 publications

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

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

The role of Notch in patterning the human vertebral column

Ameliorating effects of curcumin on nicotine-induced mice testes

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