Abstract

Lead is a public health hazard substance affecting millions of people worldwide especially those who are occupationally exposed. Our study aimed to investigate the effect of occupational lead exposure on mitochondria DNA (mtDNA). By sequencing the whole mitochondria genome, we identified 25 unique variants in lead exposed subjects affecting 10 protein coding genes in the order of MT-ND1, MT-ND2, MT-CO2, MT-ATP8, MT-ATP6, MT-CO3, MT-ND3, MT-ND4, MT-ND5, and MT-CYB. Mitochondria functional analysis revealed that exposure to lead can reduce reactive oxygen species (ROS) levels, alter mitochondria membrane potential (MMP) and increase mitochondrial mass (MM). This was further supported by mtDNA copy number analysis which was increased in lead exposed individuals compared to unexposed control group indicating the compensatory mechanism that lead has in stabilizing the mitochondria. This is the first report of mtDNA mutation and copy number analysis in occupationally lead exposed subjects where we identified mtDNA mutation signature associated with lead exposure thus providing evidence for altered molecular mechanism to compensate mitochondrial oxidative stress.

Original languageEnglish
Pages (from-to)60-66
Number of pages7
JournalMitochondrion
Volume48
DOIs
Publication statusPublished - 01-09-2019

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Mitochondria
Genome
DNA
Mutation
Gene Order
Mitochondrial Membrane Potential
Occupational Exposure
Lead
Reactive Oxygen Species
Oxidative Stress
Public Health
Control Groups
Proteins

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology

Cite this

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title = "Whole mitochondria genome mutational spectrum in occupationally exposed lead subjects",
abstract = "Lead is a public health hazard substance affecting millions of people worldwide especially those who are occupationally exposed. Our study aimed to investigate the effect of occupational lead exposure on mitochondria DNA (mtDNA). By sequencing the whole mitochondria genome, we identified 25 unique variants in lead exposed subjects affecting 10 protein coding genes in the order of MT-ND1, MT-ND2, MT-CO2, MT-ATP8, MT-ATP6, MT-CO3, MT-ND3, MT-ND4, MT-ND5, and MT-CYB. Mitochondria functional analysis revealed that exposure to lead can reduce reactive oxygen species (ROS) levels, alter mitochondria membrane potential (MMP) and increase mitochondrial mass (MM). This was further supported by mtDNA copy number analysis which was increased in lead exposed individuals compared to unexposed control group indicating the compensatory mechanism that lead has in stabilizing the mitochondria. This is the first report of mtDNA mutation and copy number analysis in occupationally lead exposed subjects where we identified mtDNA mutation signature associated with lead exposure thus providing evidence for altered molecular mechanism to compensate mitochondrial oxidative stress.",
author = "Mani, {Monica Shirley} and Sanjiban Chakrabarty and Mallya, {Sandeep P.} and Kabekkodu, {Shama Prasada} and Pradyumna Jayaram and Varghese, {Vinay Koshy} and Dsouza, {Herman Sunil} and Kapaettu Satyamoorthy",
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Whole mitochondria genome mutational spectrum in occupationally exposed lead subjects. / Mani, Monica Shirley; Chakrabarty, Sanjiban; Mallya, Sandeep P.; Kabekkodu, Shama Prasada; Jayaram, Pradyumna; Varghese, Vinay Koshy; Dsouza, Herman Sunil; Satyamoorthy, Kapaettu.

In: Mitochondrion, Vol. 48, 01.09.2019, p. 60-66.

Research output: Contribution to journalArticle

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AU - Chakrabarty, Sanjiban

AU - Mallya, Sandeep P.

AU - Kabekkodu, Shama Prasada

AU - Jayaram, Pradyumna

AU - Varghese, Vinay Koshy

AU - Dsouza, Herman Sunil

AU - Satyamoorthy, Kapaettu

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N2 - Lead is a public health hazard substance affecting millions of people worldwide especially those who are occupationally exposed. Our study aimed to investigate the effect of occupational lead exposure on mitochondria DNA (mtDNA). By sequencing the whole mitochondria genome, we identified 25 unique variants in lead exposed subjects affecting 10 protein coding genes in the order of MT-ND1, MT-ND2, MT-CO2, MT-ATP8, MT-ATP6, MT-CO3, MT-ND3, MT-ND4, MT-ND5, and MT-CYB. Mitochondria functional analysis revealed that exposure to lead can reduce reactive oxygen species (ROS) levels, alter mitochondria membrane potential (MMP) and increase mitochondrial mass (MM). This was further supported by mtDNA copy number analysis which was increased in lead exposed individuals compared to unexposed control group indicating the compensatory mechanism that lead has in stabilizing the mitochondria. This is the first report of mtDNA mutation and copy number analysis in occupationally lead exposed subjects where we identified mtDNA mutation signature associated with lead exposure thus providing evidence for altered molecular mechanism to compensate mitochondrial oxidative stress.

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