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035 a| (OCoLC)1456021973;

090 a| QD341.A6;

049 a| EREE;

100 1 a| Yan, Lisa,e| author.?| UNAUTHORIZED;

245 10 a| Chronic low dose toxicity of acrolein in C. elegans mitochondria /c| by Lisa Yan.;

264 1 a| [Greenville, N.C.] :b| [East Carolina University],c| 2024.;

300 a| 1 online resource (92 pages) :b| illustrations (chiefly color);

336 a| textb| txt2| rdacontent;

337 a| computerb| c2| rdamedia;

338 a| online resourceb| cr2| rdacarrier;

347 a| text fileb| application/pdfc| 1.62 MB2| rda;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| M.S.c| East Carolina Universityd| 2024.;

500 a| Presented to the Faculty of the Department of Biology;

500 a| Advisor: Eric Anderson;

500 a| Title from PDF t.p. (viewed February 5, 2026).;

520 3 a| Acrolein (ACR) is a chemical of interest in the pathology and progression of mitochondrial disease and disorder. Chemical exposure to ACR may occur exogenously due to the use of herbicides or burning of fossil fuels, or endogenously as a by-product from various metabolic pathways. Several studies focus on the impact of high dose acute exposure of ACR with various model organisms, including live rats and mice, human spermatozoa, and several cell culture models. These models do not address the consequences of long term or chronic, low dose exposures and impacts on progeny. For these reasons, the model C. elegans was ideal because of its established genome, ability to self-fertilize or sexually reproduce, ability to yield three hundred progenies in its lifetime, and its short and understood lifespan. We hypothesized that C. elegans would experience mitochondrial dysfunction when chronically exposed to low doses of ACR, particularly with the 15 [mu]M concentration. Based on previous research indicating another electrophilic aldehyde, 4-hydroxynonenal (4-HNE) inhibits SDH activity by forming a protein adduct with the redox subunit of SDH, we predicted that ACR may inhibit complex II (SDH) activity through protein adduct formation. We also predicted that ACR may also decrease lifespan and fecundity across generations of nematodes. To test our hypothesis and aims, we utilized C. elegans in experiments incorporating lifespan and fecundity assays, performed a histochemical stain to qualitatively measure SDH activity, used RT-PCR targeting specific genes related to oxidative stress and SDHA-1, and attempted to isolate mitochondria to perform SDH activity assays measured with spectrophotometry. Our results from the lifespan and fecundity assays suggested that low dose, chronic ACR exposure may decrease lifespan and fecundity in C. elegans. We also learned that C. elegans will attempt to leave the agar plate at ACR concentrations of 75 [mu]M and 100 [mu]M. Our RT-PCR results showed an upregulation in SDHA-1 and SOD-3 transcription in C. elegans after a 24-hour exposure to 100 [mu]M ACR. These results suggest that higher doses of ACR may cause oxidative stress or damage to the mitochondria and SDH. Further experimentation may help better determine the interaction between ACR and the flavonoid subunit of SDH.;

504 a| Includes bibliographical references.;

650 0 a| Acrolein.=| ^A762883;

650 0 a| Caenorhabditis elegans.=| ^A627930;

650 0 a| Succinate dehydrogenase.=| ^A1488881;

650 0 a| Mitochondrial pathology.=| ^A576127;

700 1 a| Anderson, Eric,e| degree supervisor.=| ^A696706;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/13717;

994 a| C0b| ERE;

596 a| 1 4;

998 a| 6477473;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 6477473-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 9/16/2024x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 6477473-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 9/16/2024x| ETDz| HERESOURCE;

Chronic low dose toxicity of acrolein in C. elegans mitochondria / by Lisa Yan.

Author/creator	Yan, Lisa author.
Other author	Anderson, Eric, degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2024.
Description	1 online resource (92 pages) : illustrations (chiefly color)
Supplemental Content	Access via ScholarShip
Subjects	Acrolein. Caenorhabditis elegans. Succinate dehydrogenase. Mitochondrial pathology.

Summary	Acrolein (ACR) is a chemical of interest in the pathology and progression of mitochondrial disease and disorder. Chemical exposure to ACR may occur exogenously due to the use of herbicides or burning of fossil fuels, or endogenously as a by-product from various metabolic pathways. Several studies focus on the impact of high dose acute exposure of ACR with various model organisms, including live rats and mice, human spermatozoa, and several cell culture models. These models do not address the consequences of long term or chronic, low dose exposures and impacts on progeny. For these reasons, the model C. elegans was ideal because of its established genome, ability to self-fertilize or sexually reproduce, ability to yield three hundred progenies in its lifetime, and its short and understood lifespan. We hypothesized that C. elegans would experience mitochondrial dysfunction when chronically exposed to low doses of ACR, particularly with the 15 [mu]M concentration. Based on previous research indicating another electrophilic aldehyde, 4-hydroxynonenal (4-HNE) inhibits SDH activity by forming a protein adduct with the redox subunit of SDH, we predicted that ACR may inhibit complex II (SDH) activity through protein adduct formation. We also predicted that ACR may also decrease lifespan and fecundity across generations of nematodes. To test our hypothesis and aims, we utilized C. elegans in experiments incorporating lifespan and fecundity assays, performed a histochemical stain to qualitatively measure SDH activity, used RT-PCR targeting specific genes related to oxidative stress and SDHA-1, and attempted to isolate mitochondria to perform SDH activity assays measured with spectrophotometry. Our results from the lifespan and fecundity assays suggested that low dose, chronic ACR exposure may decrease lifespan and fecundity in C. elegans. We also learned that C. elegans will attempt to leave the agar plate at ACR concentrations of 75 [mu]M and 100 [mu]M. Our RT-PCR results showed an upregulation in SDHA-1 and SOD-3 transcription in C. elegans after a 24-hour exposure to 100 [mu]M ACR. These results suggest that higher doses of ACR may cause oxidative stress or damage to the mitochondria and SDH. Further experimentation may help better determine the interaction between ACR and the flavonoid subunit of SDH.
General note	Presented to the Faculty of the Department of Biology
General note	Advisor: Eric Anderson
General note	Title from PDF t.p. (viewed February 5, 2026).
Dissertation note	M.S. East Carolina University 2024.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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Chronic low dose toxicity of acrolein in C. elegans mitochondria / by Lisa Yan.

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