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Chemically Induced Toxicity at the R...

Fritsch, Erika Beth.

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Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species./
Author:	Fritsch, Erika Beth.
Description:	125 p.
Notes:	Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.
Contained By:	Dissertation Abstracts International75-01B(E).
Subject:	Health Sciences, Toxicology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3596874
ISBN:	9781303442520

Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species.
Fritsch, Erika Beth.

Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species. - 125 p.

Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.

Thesis (Ph.D.)--University of California, Davis, 2013.

In aquatic toxicology, swimming is a sublethal indicator of chemically induced stress because it can describe both intra/interspecies interactions and has been correlated with ecological fitness. However, there is currently a lack of information regarding chemicals that affect the physiological process that underlies swimming performance in fish, namely locomotion. Two receptors essential for coordinated locomotion are the voltage sensitive L-type Ca2+ channel (i.e. dihydropyridine receptor; DHPR) on the plasma membrane and the Ca2+ release channel (ryanodine receptor; RyR) embedded within the sarcoplasmic reticulum of striated muscle. As the functional basis of excitation-contraction coupling, and numerous other physiological processes, DHPRs and RyRs are often the target of research addressing their role in genetically or environmentally induced disease states. However, studies regarding chemically induced Ca2+ signaling disruption due to altered DHPR or RyR function, or the fidelity of their interactions, has been limited to mammals and the link between "receptor" toxicity and animal performance is poorly understood. The current research investigated whether common aquatic contaminants disrupt the RyR and/or DHPR in teleost and whether receptor based toxicity is linked to changes at the whole organism or population level. Work demonstrated that environmentally relevant concentrations of non-dioxin-like polychlorinated biphenyls (NDL PCBs) enhance the activity of the RyR, isoform 1, in rainbow trout (Oncorhynchus mykiss) skeletal muscle. The structurally similar antibacterial agent triclosan was found to inhibit the DHPR in fathead minnow (Pimephales promelas) and changes in DHPR-RyR related mRNA and protein levels correlated with altered swimming and survival indexes in exposed minnow. Finally, chronic exposure to NDL PCBs may have resulted in environmentally and genetically based adaptations in the RyR related pathway of Atlantic killifish (Fundulus heteroclitus ) from the PCB contaminated US EPA Superfund Site at New Bedford Harbor (MA). This research demonstrates that both legacy and current use contaminants of concern alter the function of the DHPR and RyR at a molecular level in teleost. More concerning, these results suggest that short exposure to RyR or DHPR chemical disruptors likely alters organismal performance and chronically exposed populations may have evolved differential Ca2+ signaling dynamics with unknown costs to other physiological systems.

ISBN: 9781303442520Subjects--Topical Terms:

1017752
Health Sciences, Toxicology.

Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species.
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245 1 0 $a Chemically Induced Toxicity at the Ryanodine Receptor and Dihydropyridine Receptor in Teleost Species.
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502 $a Thesis (Ph.D.)--University of California, Davis, 2013.
520 $a In aquatic toxicology, swimming is a sublethal indicator of chemically induced stress because it can describe both intra/interspecies interactions and has been correlated with ecological fitness. However, there is currently a lack of information regarding chemicals that affect the physiological process that underlies swimming performance in fish, namely locomotion. Two receptors essential for coordinated locomotion are the voltage sensitive L-type Ca2+ channel (i.e. dihydropyridine receptor; DHPR) on the plasma membrane and the Ca2+ release channel (ryanodine receptor; RyR) embedded within the sarcoplasmic reticulum of striated muscle. As the functional basis of excitation-contraction coupling, and numerous other physiological processes, DHPRs and RyRs are often the target of research addressing their role in genetically or environmentally induced disease states. However, studies regarding chemically induced Ca2+ signaling disruption due to altered DHPR or RyR function, or the fidelity of their interactions, has been limited to mammals and the link between "receptor" toxicity and animal performance is poorly understood. The current research investigated whether common aquatic contaminants disrupt the RyR and/or DHPR in teleost and whether receptor based toxicity is linked to changes at the whole organism or population level. Work demonstrated that environmentally relevant concentrations of non-dioxin-like polychlorinated biphenyls (NDL PCBs) enhance the activity of the RyR, isoform 1, in rainbow trout (Oncorhynchus mykiss) skeletal muscle. The structurally similar antibacterial agent triclosan was found to inhibit the DHPR in fathead minnow (Pimephales promelas) and changes in DHPR-RyR related mRNA and protein levels correlated with altered swimming and survival indexes in exposed minnow. Finally, chronic exposure to NDL PCBs may have resulted in environmentally and genetically based adaptations in the RyR related pathway of Atlantic killifish (Fundulus heteroclitus ) from the PCB contaminated US EPA Superfund Site at New Bedford Harbor (MA). This research demonstrates that both legacy and current use contaminants of concern alter the function of the DHPR and RyR at a molecular level in teleost. More concerning, these results suggest that short exposure to RyR or DHPR chemical disruptors likely alters organismal performance and chronically exposed populations may have evolved differential Ca2+ signaling dynamics with unknown costs to other physiological systems.
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