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Perinatal tobacco smoke exposure increases vascular oxidative stress and mitochondrial damage in non-human primates.

Westbrook DG, Anderson PG, Pinkerton KE, Ballinger SW - Cardiovasc. Toxicol. (2010)

Bottom Line: Epidemiological studies suggest that events occurring during fetal and early childhood development influence disease susceptibility.M. mulatta were exposed to low levels of ETS (1 mg/m(3) total suspended particulates) from gestation (day 40) to early childhood (1 year), and aortic tissues were assessed for oxidized proteins (protein carbonyls), antioxidant activity (SOD), mitochondrial function (cytochrome oxidase), and mitochondrial damage (mitochondrial DNA damage).Results revealed that perinatal ETS exposure resulted in significantly increased oxidative stress, mitochondrial dysfunction and damage which were accompanied by significantly decreased mitochondrial antioxidant capacity and mitochondrial copy number in vascular tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, VH G019F, 1530 3rd Avenue S., Birmingham, AL 35294-0019, USA.

ABSTRACT
Epidemiological studies suggest that events occurring during fetal and early childhood development influence disease susceptibility. Similarly, molecular studies in mice have shown that in utero exposure to cardiovascular disease (CVD) risk factors such as environmental tobacco smoke (ETS) increased adult atherogenic susceptibility and mitochondrial damage; however, the molecular effects of similar exposures in primates are not yet known. To determine whether perinatal ETS exposure increased mitochondrial damage, dysfunction and oxidant stress in primates, archived tissues from the non-human primate model Macaca mulatta (M. mulatta) were utilized. M. mulatta were exposed to low levels of ETS (1 mg/m(3) total suspended particulates) from gestation (day 40) to early childhood (1 year), and aortic tissues were assessed for oxidized proteins (protein carbonyls), antioxidant activity (SOD), mitochondrial function (cytochrome oxidase), and mitochondrial damage (mitochondrial DNA damage). Results revealed that perinatal ETS exposure resulted in significantly increased oxidative stress, mitochondrial dysfunction and damage which were accompanied by significantly decreased mitochondrial antioxidant capacity and mitochondrial copy number in vascular tissue. Increased mitochondrial damage was also detected in buffy coat tissues in exposed M. mulatta. These studies suggest that perinatal tobacco smoke exposure increases vascular oxidative stress and mitochondrial damage in primates, potentially increasing adult disease susceptibility.

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Cytochrome oxidase (complex IV) activity in M. mulatta. Complex IV activity was determined from mitochondrial isolates extracted from aortic tissues. Unexposed, M. mulatta age-matched control; ETS, M. mulatta exposed to 1 mg/m3 ETS during gestation to 1 year of age. Asterisks indicate significant difference (P < 0.05) from unexposed M. mulatta (n = 3/group/tissue)
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Fig6: Cytochrome oxidase (complex IV) activity in M. mulatta. Complex IV activity was determined from mitochondrial isolates extracted from aortic tissues. Unexposed, M. mulatta age-matched control; ETS, M. mulatta exposed to 1 mg/m3 ETS during gestation to 1 year of age. Asterisks indicate significant difference (P < 0.05) from unexposed M. mulatta (n = 3/group/tissue)

Mentions: To determine whether these changes in mtDNA integrity were associated with altered mitochondrial function in M. mulatta exposed to perinatal ETS, cytochrome oxidase (complex IV) activity was determined from aortic samples. Figure 6 reveals that mitochondrial function was significantly declined in M. mulatta sustaining perinatal exposure to ETS compared to unexposed controls.Fig. 6


Perinatal tobacco smoke exposure increases vascular oxidative stress and mitochondrial damage in non-human primates.

Westbrook DG, Anderson PG, Pinkerton KE, Ballinger SW - Cardiovasc. Toxicol. (2010)

Cytochrome oxidase (complex IV) activity in M. mulatta. Complex IV activity was determined from mitochondrial isolates extracted from aortic tissues. Unexposed, M. mulatta age-matched control; ETS, M. mulatta exposed to 1 mg/m3 ETS during gestation to 1 year of age. Asterisks indicate significant difference (P < 0.05) from unexposed M. mulatta (n = 3/group/tissue)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2926475&req=5

Fig6: Cytochrome oxidase (complex IV) activity in M. mulatta. Complex IV activity was determined from mitochondrial isolates extracted from aortic tissues. Unexposed, M. mulatta age-matched control; ETS, M. mulatta exposed to 1 mg/m3 ETS during gestation to 1 year of age. Asterisks indicate significant difference (P < 0.05) from unexposed M. mulatta (n = 3/group/tissue)
Mentions: To determine whether these changes in mtDNA integrity were associated with altered mitochondrial function in M. mulatta exposed to perinatal ETS, cytochrome oxidase (complex IV) activity was determined from aortic samples. Figure 6 reveals that mitochondrial function was significantly declined in M. mulatta sustaining perinatal exposure to ETS compared to unexposed controls.Fig. 6

Bottom Line: Epidemiological studies suggest that events occurring during fetal and early childhood development influence disease susceptibility.M. mulatta were exposed to low levels of ETS (1 mg/m(3) total suspended particulates) from gestation (day 40) to early childhood (1 year), and aortic tissues were assessed for oxidized proteins (protein carbonyls), antioxidant activity (SOD), mitochondrial function (cytochrome oxidase), and mitochondrial damage (mitochondrial DNA damage).Results revealed that perinatal ETS exposure resulted in significantly increased oxidative stress, mitochondrial dysfunction and damage which were accompanied by significantly decreased mitochondrial antioxidant capacity and mitochondrial copy number in vascular tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, VH G019F, 1530 3rd Avenue S., Birmingham, AL 35294-0019, USA.

ABSTRACT
Epidemiological studies suggest that events occurring during fetal and early childhood development influence disease susceptibility. Similarly, molecular studies in mice have shown that in utero exposure to cardiovascular disease (CVD) risk factors such as environmental tobacco smoke (ETS) increased adult atherogenic susceptibility and mitochondrial damage; however, the molecular effects of similar exposures in primates are not yet known. To determine whether perinatal ETS exposure increased mitochondrial damage, dysfunction and oxidant stress in primates, archived tissues from the non-human primate model Macaca mulatta (M. mulatta) were utilized. M. mulatta were exposed to low levels of ETS (1 mg/m(3) total suspended particulates) from gestation (day 40) to early childhood (1 year), and aortic tissues were assessed for oxidized proteins (protein carbonyls), antioxidant activity (SOD), mitochondrial function (cytochrome oxidase), and mitochondrial damage (mitochondrial DNA damage). Results revealed that perinatal ETS exposure resulted in significantly increased oxidative stress, mitochondrial dysfunction and damage which were accompanied by significantly decreased mitochondrial antioxidant capacity and mitochondrial copy number in vascular tissue. Increased mitochondrial damage was also detected in buffy coat tissues in exposed M. mulatta. These studies suggest that perinatal tobacco smoke exposure increases vascular oxidative stress and mitochondrial damage in primates, potentially increasing adult disease susceptibility.

Show MeSH
Related in: MedlinePlus