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Kinetics of Mercury Uptake by Juvenile Fish

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Date Issued:
2018-07-16
Abstract/Description:
Increased mercury (Hg) emissions have become a widespread issue in the environment due to its long atmospheric residence time and potential for methylation in aquatic environments following deposition. Animals in aquatic environments are particularly vulnerable to toxicity due to high deposition and the capability of Hg to easily biomagnify through trophic levels. Diet is the primary pathway of Hg exposure as compared to water; leaving piscivorous species at higher risk of exposure and toxicity. To examine kinetics of Hg uptake and subsequent distribution among tissue, a model fish was fed tissues from wild-caught higher trophic level fish with naturally incorporated Hg. Unexpectedly, the model redfish began dying early in the experiment. However, the mortality was not dose dependent and, thus, did not appear to be due to Hg. While other factors such as poor water quality, lack of nutrients in the experimental diet, and various toxins (e.g., ciguatoxins, brevetoxins, and composite cytotoxicity) were also ruled out, the cause of the mortality remains unknown. Although mortality was a source of uncertainty over the course of the exposure, Hg accumulated in the redfish in a dose-dependent manner. Potential steady-state of the redfish whole-body Hg concentration was assessed using a model derived from published literature. The model was effective in its ability to predict steady-state Hg concentrations that corresponded to the observed levels in the model redfish. Uptake kinetics was further studied by analyzing Hg distribution in the redfish. Mercury in ingested food was assumed to be taken up by the redfish intestinal tissue and distributed to the rest of the body in stages, as seen by the various Hg concentrations measured in the tissues over time. During periods of high exposure, Hg accumulated in the Liver>Muscle>Brain>Eyes, and Muscle>Liver>Brain>Eyes during low Hg exposure. The agreement between these results and the published literature suggests that the high mortality of redfish early in the experiment did not have a large effect on the Hg kinetics and assessment of the steady-state model.
Title: Kinetics of Mercury Uptake by Juvenile Fish.
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Name(s): Godwin, Jessica Ann, author
Type of Resource: text
Genre: Thesis
Issuance: single unit
Date Issued: 2018-07-16
Physical Form: PDF
Extent: 42 pgs.
Language(s): English
eng
Abstract/Description: Increased mercury (Hg) emissions have become a widespread issue in the environment due to its long atmospheric residence time and potential for methylation in aquatic environments following deposition. Animals in aquatic environments are particularly vulnerable to toxicity due to high deposition and the capability of Hg to easily biomagnify through trophic levels. Diet is the primary pathway of Hg exposure as compared to water; leaving piscivorous species at higher risk of exposure and toxicity. To examine kinetics of Hg uptake and subsequent distribution among tissue, a model fish was fed tissues from wild-caught higher trophic level fish with naturally incorporated Hg. Unexpectedly, the model redfish began dying early in the experiment. However, the mortality was not dose dependent and, thus, did not appear to be due to Hg. While other factors such as poor water quality, lack of nutrients in the experimental diet, and various toxins (e.g., ciguatoxins, brevetoxins, and composite cytotoxicity) were also ruled out, the cause of the mortality remains unknown. Although mortality was a source of uncertainty over the course of the exposure, Hg accumulated in the redfish in a dose-dependent manner. Potential steady-state of the redfish whole-body Hg concentration was assessed using a model derived from published literature. The model was effective in its ability to predict steady-state Hg concentrations that corresponded to the observed levels in the model redfish. Uptake kinetics was further studied by analyzing Hg distribution in the redfish. Mercury in ingested food was assumed to be taken up by the redfish intestinal tissue and distributed to the rest of the body in stages, as seen by the various Hg concentrations measured in the tissues over time. During periods of high exposure, Hg accumulated in the Liver>Muscle>Brain>Eyes, and Muscle>Liver>Brain>Eyes during low Hg exposure. The agreement between these results and the published literature suggests that the high mortality of redfish early in the experiment did not have a large effect on the Hg kinetics and assessment of the steady-state model.
Identifier: fgcu_ETD_0246 (IID)
Note(s): Degree Awarded: Master of Science
Subject(s): Kinetics
Mercury
Model
Steady-state
Persistent Link to This Record: http://purl.flvc.org/fgcu/fd/fgcu_ETD_0246
Use and Reproduction: Creator holds copyright.
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FGCU