Changes in the levels of l -carnitine, acetyl- l -carnitine and propionyl- l -carnitine are involved in perfluorooctanoic acid induced developmental cardiotoxicity in chicken embryo

Jiang, Qixiao; Wang, Chunbo; Xue, Chan; Xue, Lingfang; Wang, Meiting; Li, Changhao; Deng, Ziwen; Wang, Qian

doi:10.1016/j.etap.2016.10.017

Cited by 13 publications

(11 citation statements)

References 45 publications

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“…The effects of l -carnitine were also investigated, whose protective effects have been reported previously [14]. In the current study, no significant differences in the ROS and NO levels were observed in the early stage embryo hearts, but our results indicated that ROS and NO might play important roles in late stage embryo hearts, which were associated with NF-κB p65 and iNOS.…”

Section: Discussionsupporting

confidence: 75%

“…In previous studies, PFOA has been associated with developmental cardiotoxicity in chicken embryos, in terms of an altered morphology and function, which was achieved at an exposure level comparable to those of an occupationally exposed human [12], suggesting the human health relevancy and need for further mechanistic studies. Interestingly, the commonly-accepted mechanism of action for PFOA, PPAR α activation, failed to explain most of the observed effects [13,14]. Meanwhile, a nutrient, l -carnitine, was found to be quite effective against such changes [14], which was consistent with various reports that l -carnitine may protect the heart [17,18].…”

Section: Discussionsupporting

confidence: 66%

“…Interestingly, the commonly-accepted mechanism of action for PFOA, PPAR α activation, failed to explain most of the observed effects [13,14]. Meanwhile, a nutrient, l -carnitine, was found to be quite effective against such changes [14], which was consistent with various reports that l -carnitine may protect the heart [17,18]. In the current study, such protection was once again confirmed, as l -carnitine co-treatment reverted the heart rate elevation induced by PFOA in hatchling chickens, thus suggesting its potential to be utilized in cardiovascular development protection.…”

Section: Discussionmentioning

confidence: 99%

“…l -carnitine is known to be cardiac protective against both chemotherapeutic agents [17] and congenital cardiomyopathy [18]. In our previous study [14], developmental exposure to PFOA decreased the l -carnitine, acetyl- l -carnitine, and propionyl- l -carnitine levels in chicken embryo and hatchling chicken hearts, while the extragenous supplement of l -carnitine effectively reverted PFOA-induced developmental cardiotoxicity. l -carnitine definitely plays a role in heart development, and has the potential to serve as a prophylaxis agent to improve public cardiovascular health.…”

Section: Introductionmentioning

confidence: 97%

“…An altered chicken cardiac function and morphology were observed in chicken embryo hearts developmentally exposed to PFOA, which were partially associated with PPAR α and BMP2 signaling [13]. Recently, decreased l -carnitine and its short-chain derivatives levels were also associated with such effects [14]. Considering the ubiquitous presence of PFOA in the environment and biota [15], such effects could be affecting the cardiovascular health of the general population and are worth further investigation.…”

Section: Introductionmentioning

confidence: 99%

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The Roles of Reactive Oxygen Species and Nitric Oxide in Perfluorooctanoic Acid-Induced Developmental Cardiotoxicity and l-Carnitine Mediated Protection

Zhao

Jiang

Wang

et al. 2017

IJMS

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Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects of l-carnitine, fertile chicken eggs were exposed to PFOA via an air cell injection, with or without l-carnitine co-treatment. The ROS and NO levels in chicken embryo hearts were determined with electron spin resonance (ESR), and the protein levels of the nuclear factor κ-light chain-enhancer of activated B cells (NF-κB) p65 and inducible nitric oxide synthase (iNOS) in chicken embryo hearts were assessed with western blotting. The results of ESR indicated that PFOA exposure induced an elevation in the ROS levels in ED19 chicken embryo hearts and hatchling chicken hearts, while l-carnitine could alleviate such changes. Meanwhile, increased NO levels were observed in ED19 embryo hearts and hatchling hearts following PFOA exposure, while l-carnitine co-treatment exerted modulatory effects. Western blotting revealed that p65 translocation in ED19 embryo hearts and hatchling hearts was enhanced by PFOA, while l-carnitine co-treatment alleviated such changes. iNOS expression levels in ED19 embryo hearts followed the same pattern as NO levels, while a suppression of expression was observed in hatchling hearts exposed to PFOA. ROS/NF-κB p65 and iNOS/NO seem to be involved in the late stage (ED19 and post hatch) of PFOA-induced developmental cardiotoxicity in a chicken embryo. l-carnitine could exert anti-oxidant and NO modulatory effects in the developing chicken embryo hearts, which likely contribute to its cardioprotective effects.

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Section: Discussionsupporting

confidence: 75%