Presenter Major
Biology
Presentation Type
Oral
Location
Hays Theatre, Wilbur Arts Building
Start Date
26-4-2024 10:20 AM
End Date
26-4-2024 10:25 AM
Description (Abstract)
Note: Z'Dhanne is a current Molloy student and conducted this research while studying at Columbia University - Mailman School of Public Health
Abstract
Background and Purpose: Mitochondrial health plays a vital role in the development of chronic health conditions, including neurodegenerative and cardiovascular diseases. Mitochondria have the unique ability to independently control replication of mitochondrial DNA (mtDNA) depending on conditions of cellular stress, including oxidative stress. Exposure to environmental metals affects a variety of health outcomes via oxidative stress pathways. Our objective was to determine the association between prenatal exposure to metals on two biomarkers of mtDNA in child blood: cellular mitochondrial DNA copy number (mtDNAcn) and cell-free mitochondria (cf-mtDNA) copy number. These two commonly investigated biomarkers in environmental exposures may represent different stress response pathways following metals exposure.
Methods: In this pilot project, whole blood and serum samples were collected at age 5 from the Columbia Children’s Center for Environmental Health Sibling-Hermanos birth cohort study made up of Dominican and African American children from Northern Manhattan (N=31). mtDNA copy number in buffy coat DNA and in serum cell-free DNA was quantified with a qRT- PCR-based protocol expressed as the ratio between a mtDNA gene (mtND1) and a nuclear DNA (nDNA) gene (B2M) to estimate mtDNA content per cell. Inductively coupled plasma-mass spectrometry was used to quantify 13 essential and nonessential metals (arsenic, barium, cesium, cobalt, copper, iron, lead, manganese, mercury, selenium, strontium, vanadium, and zinc) in umbilical cord blood. Linear regression models were used to estimate the associations between individual metals and mtDNA biomarkers adjusting for age at measurement, race/ethnicity, and parity.
Results: Umbilical cord copper levels were significantly negatively associated with a reduction in cellular mtDNAcn [-0.0015 (-0.003, -3.4e-5) per µg/L increase in copper, p = 0.05] and positively associated with cf-mtDNA (0.96 (-0.06, 2.0) increase in the ratio of cf-mtDNA to cf- nDNA per µg/L increase in copper, p = 0.06). Mean copper levels were 743 ± 91.0 µg/L. No associations between mtDNA biomarkers and other metals were observed.
Conclusions: In this preliminary analysis, copper levels at birth were associated with cellular and cell-free mtDNA biomarkers in opposing directions during childhood. Copper is an essential metal for child development, suggesting a complex relationship between prenatal copper and mitochondrial health.
Keywords
Mitochondria, Neurodevelopment, qPCR, cf-mtDNA, mtDNA, biomarkers
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Related Pillar(s)
Community, Service
Included in
Community Health and Preventive Medicine Commons, Environmental Public Health Commons, Maternal and Child Health Commons, Other Public Health Commons
Investigating the Influence of Prenatal Metals Exposures on Childhood Mitochondrial Biomarkers
Hays Theatre, Wilbur Arts Building
Note: Z'Dhanne is a current Molloy student and conducted this research while studying at Columbia University - Mailman School of Public Health
Abstract
Background and Purpose: Mitochondrial health plays a vital role in the development of chronic health conditions, including neurodegenerative and cardiovascular diseases. Mitochondria have the unique ability to independently control replication of mitochondrial DNA (mtDNA) depending on conditions of cellular stress, including oxidative stress. Exposure to environmental metals affects a variety of health outcomes via oxidative stress pathways. Our objective was to determine the association between prenatal exposure to metals on two biomarkers of mtDNA in child blood: cellular mitochondrial DNA copy number (mtDNAcn) and cell-free mitochondria (cf-mtDNA) copy number. These two commonly investigated biomarkers in environmental exposures may represent different stress response pathways following metals exposure.
Methods: In this pilot project, whole blood and serum samples were collected at age 5 from the Columbia Children’s Center for Environmental Health Sibling-Hermanos birth cohort study made up of Dominican and African American children from Northern Manhattan (N=31). mtDNA copy number in buffy coat DNA and in serum cell-free DNA was quantified with a qRT- PCR-based protocol expressed as the ratio between a mtDNA gene (mtND1) and a nuclear DNA (nDNA) gene (B2M) to estimate mtDNA content per cell. Inductively coupled plasma-mass spectrometry was used to quantify 13 essential and nonessential metals (arsenic, barium, cesium, cobalt, copper, iron, lead, manganese, mercury, selenium, strontium, vanadium, and zinc) in umbilical cord blood. Linear regression models were used to estimate the associations between individual metals and mtDNA biomarkers adjusting for age at measurement, race/ethnicity, and parity.
Results: Umbilical cord copper levels were significantly negatively associated with a reduction in cellular mtDNAcn [-0.0015 (-0.003, -3.4e-5) per µg/L increase in copper, p = 0.05] and positively associated with cf-mtDNA (0.96 (-0.06, 2.0) increase in the ratio of cf-mtDNA to cf- nDNA per µg/L increase in copper, p = 0.06). Mean copper levels were 743 ± 91.0 µg/L. No associations between mtDNA biomarkers and other metals were observed.
Conclusions: In this preliminary analysis, copper levels at birth were associated with cellular and cell-free mtDNA biomarkers in opposing directions during childhood. Copper is an essential metal for child development, suggesting a complex relationship between prenatal copper and mitochondrial health.
