Limits...
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.

Show MeSH

Related in: MedlinePlus

Histopathology of abdominal aorta from M. mulatta. Histopathology of H&E-stained section of abdominal aorta shows accumulation of inflammatory cells with widening of the subintimal region (arrows) in the ETS-exposed animal (b) versus age-matched control aorta (a). Magnification bar (inset on panel b) is 50 μM. Bar graph (c) depicts mean cellularity score ± SEM (see “Methods”), showing that a significant difference exists between unexposed and ETS-exposed (perinatal) animals
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2926475&req=5

Fig7: Histopathology of abdominal aorta from M. mulatta. Histopathology of H&E-stained section of abdominal aorta shows accumulation of inflammatory cells with widening of the subintimal region (arrows) in the ETS-exposed animal (b) versus age-matched control aorta (a). Magnification bar (inset on panel b) is 50 μM. Bar graph (c) depicts mean cellularity score ± SEM (see “Methods”), showing that a significant difference exists between unexposed and ETS-exposed (perinatal) animals

Mentions: Finally, to determine whether these observed changes in molecular biology were also accompanied by differences in histology, archived tissues were fixed, sectioned and stained with hematoxylin-eosin, and provided to a trained pathologist in a blinded fashion for scoring. Results showed that perinatal exposure to ETS was associated with significantly increased numbers of cells within the subintima, indicative of early atherogenic changes in the abdominal aorta compared to age-matched controls (Fig. 7). Consequently, both changes at the molecular and cellular levels appear to be associated with perinatal ETS exposure in M. mulatta.Fig. 7


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)

Histopathology of abdominal aorta from M. mulatta. Histopathology of H&E-stained section of abdominal aorta shows accumulation of inflammatory cells with widening of the subintimal region (arrows) in the ETS-exposed animal (b) versus age-matched control aorta (a). Magnification bar (inset on panel b) is 50 μM. Bar graph (c) depicts mean cellularity score ± SEM (see “Methods”), showing that a significant difference exists between unexposed and ETS-exposed (perinatal) animals
© Copyright Policy
Related In: Results  -  Collection

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

Fig7: Histopathology of abdominal aorta from M. mulatta. Histopathology of H&E-stained section of abdominal aorta shows accumulation of inflammatory cells with widening of the subintimal region (arrows) in the ETS-exposed animal (b) versus age-matched control aorta (a). Magnification bar (inset on panel b) is 50 μM. Bar graph (c) depicts mean cellularity score ± SEM (see “Methods”), showing that a significant difference exists between unexposed and ETS-exposed (perinatal) animals
Mentions: Finally, to determine whether these observed changes in molecular biology were also accompanied by differences in histology, archived tissues were fixed, sectioned and stained with hematoxylin-eosin, and provided to a trained pathologist in a blinded fashion for scoring. Results showed that perinatal exposure to ETS was associated with significantly increased numbers of cells within the subintima, indicative of early atherogenic changes in the abdominal aorta compared to age-matched controls (Fig. 7). Consequently, both changes at the molecular and cellular levels appear to be associated with perinatal ETS exposure in M. mulatta.Fig. 7

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