Abstract
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.
Highlights
Perfluorooctanoic acid (PFOA) belongs to the perfluoroalkyl acids (PFAAs) family, and is widely used in the production of myriad polymer products, such as polytetrafluoroethene (PTFE)
The results indicated that no significant changes to reactive oxygen species (ROS) levels were present in Embryonic Day 6 (ED6), 10, or 15 chicken embryo hearts (Figure 2A–C), while
The results indicated that no significant changes to ROS levels were present in ED6, 10, or 15 chicken embryo hearts (Figure 2A–C), while a a sisgingnifiifciacnant tinicnrceraesaeseininthteheRORSOlSevleevlselws awsadsedteectteecdteidn iEnDE1D9 1c9hicchkiecnkeenmebmryboryhoeahretsaratns danhdathchalticnhgling chickheicnkheneahrtesar(Ftsig(Fuirgeu2rDe,2ED).,EM).eManewanhwileh,iLle-c, aLr-cnaitrinnieticnoe-ctroe-atrtmeaetmnteenftfeecftfievcetliyverleyvreervteedrttehdetRheORSOsuSrsguerge in EinD1E9Dc1h9icckheinckeemnbermyobrhyeoarhtesa(rFtisg(uFrieg2uDre).2IDn)h. aIntchiantgchcihnigckcehnics,kaentrse,nadtroefnddecorfedaseecrweaasseowbsaesrvoebdseirnved theiLn-cthaernLi-tcinaerncioti-ntreeacotm-terenattgmroeunpt ghreoaurptshceoamrtpsacroemd ptoarthede PtoFOthAe PtrFeOatAedtrgeraotuepd hgeroaurtps,hbeuatrths,isbuwtatshnisowt as statnisotticsatalltyisstigcanlilfiycsaingtn(ipfic=a0n.t1(0p, F=i0g.u1r0e, F2iEg)u. re 2E)
Summary
Perfluorooctanoic acid (PFOA) belongs to the perfluoroalkyl acids (PFAAs) family, and is widely used in the production of myriad polymer products, such as polytetrafluoroethene (PTFE). 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 Both PFOA and L-carnitine could affect reactive oxygen species (ROS) generation and nitric oxide (NO) production [19,20]. A similar controversy applies for NO, where both an increase and decrease in NO levels were reported following L-carnitine supplementation [25,26] Such controversies highlight the need for further investigations regarding the effects of L-carnitine on ROS and NO, which may contribute to its cardiac protective effects against PFOA-induced developmental cardiotoxicity. The nuclear factor κ-light chain-enhancer of activated B cells (NF-κB) p65 and inducible nitric oxide synthase (iNOS) has been associated with such changes
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