Effect of pre- and postnatal exposure to urban air pollution on myocardial lipid peroxidation levels in adult mice

Abstract

Exposure to air pollution can elicit cardiovascular health effects. Children and unborn fetuses appear to be particularly vulnerable. However, the mechanisms involved in cardiovascular damage are poorly understood. It has been suggested that the oxidative stress generated by air pollution exposure triggers tissue injury. To investigate whether prenatal exposure can enhance oxidative stress in myocardium of adult animals, mice were placed in a clean chamber (CC, filtered urban air) and in a polluted chamber (PC, São Paulo city) during the gestational period and/or for 3 mo after birth, according to 4 protocols: control group—prenatal and postnatal life in CC; prenatal group—prenatal in PC and postnatal life in CC; postnatal group—prenatal in CC and postnatal life in PC; and pre–post group—prenatal and postnatal life in PC. As an indicator of oxidative stress, levels of lipid peroxidation in hearts were measured by malondialdehyde (MDA) quantification and by quantification of the myocardial immunoreactivity for 15-F2t-isoprostane. Ultrastructural studies were performed to detect cellular alterations related to oxidative stress. Concentration of MDA was significantly increased in postnatal (2.45 ± 0.84 nmol/mg) and pre–post groups (3.84 ± 1.39 nmol/mg) compared to the control group (0.31 ± 0.10 nmol/mg) (p < .01). MDA values in the pre–post group were significantly increased compared to the prenatal group (0.71 ± 0.15 nmol/mg) (p = .017). Myocardial isoprostane area fraction in the pre–post group was increased compared to other groups (p ≤ .01). Results show that ambient levels of air pollution elicit cardiac oxidative stress in adult mice, and that gestational exposure may enhance this effect.

Keywords::

• Air pollution
• heart
• lipid peroxidation
• mice
• oxidative stress
• particulate matter

Acknowledgements

We thank the technical staff of the Experimental Air Pollution Laboratory for animal care and PM monitoring during the exposure period of this study. We also thank Dr. Luiz Fernando Ferraz da Silva for statistical support and Angela B. G. dos Santos for help with immunohistochemical preparations. We are grateful to Loris Calzolari for preparing Figure 1.

Declaration of interest: This work was supported by grants from the State of São Paulo Research Foundation (FAPESP) and by the Laboratories of Medical Investigation (LIMs) HCFMUSP. The authors alone are responsible for the content and writing of the paper.