Effects of sulfur dioxide, ozone, and ambient air pollution on lung histopathology, oxidative-stress biomarkers, and apoptosis-related gene expressions in rats

Abstract

Purpose of the Study

Ambient air pollution (AAP) has become an important health problem globally. Besides, several pieces of evidence indicate that air pollutants such as sulfur dioxide (SO₂) and ozone (O₃) are major contributors to a wide range of non-communicable diseases. The present study investigated the effects of AAP, sulfur dioxide, and ozone on oxidative stress, histopathology, and some apoptosis-related genes expressions of lung tissue in a rat model.

Materials and Methods

Thirty-two Wistar rats were randomly divided into the control, AAP, sulfur dioxide (10 ppm), and ozone (0.6 ppm) groups. After five consecutive weeks’ exposure to the selected pollutants (3 h/day), lung tissues were harvested and immediately fixed with formalin. The samples were routinely processed, sectioned, stained with hematoxylin and eosin (H&E), and finally assessed for presence of pathological changes. Expression changes of BAX, p-53, EGFR, caspase-3, caspase-8 and caspase-9 were assayed using the RT-qPCR method. One hundred milligrams of lung tissues were extracted and the supernatants were used for assaying malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GP_X), and catalase activities.

Results

GPx activity was increased in the ozone (P = 0.05) and AAP (P < 0.001) groups and also MDA level in sulfur dioxide group (P = 0.008). Pathological lesions were mild, moderate, and severe in the sulfur dioxide, ozone, and AAP groups, respectively, as compared to control group (P ˂ 0.05). Exposure to AAP and sulfur dioxide enhanced BAX (P = 0.002) and caspase-8 (P < 0.001) mRNA expression, respectively. Caspases-3 and −8 mRNA expressions were elevated in ozone group (P < 0.001).

Conclusions

The results indicated induction of oxidative stress. Our results suggest the apoptosis stimuli effect of AAP and also the extrinsic apoptotic pathway trigger effect of sulfur dioxide and ozone in the lung tissue in the concentrations used in the present study. The histopathological and the genes expression changes may be a result of the induced oxidative stress in the lung tissues.

Keywords:

• Air pollution
• lung
• ozone
• rat
• sulfur dioxide

Acknowledgments

This article results from a research project (ID 64884) that was financing and conducted at the Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. The authors appreciate the financial and instrumental support provided by the Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran.

Authors’ contributions

Sorayya Kheirouri and Mohammad Alizadeh designed the experiment; Dariush Shanehbandi and Fateme Eskandari performed sample preparation and RT-PCR; Monireh Khordadmehr performed histopathology tests; Razieh Musapour Sultan Abad, Mohammad Alizadeh, and Mehran Mesgari-Abbasi performed animal experiments and interventions; Mehran Mesgari-Abbasi and Fateme Eskandari performed biochemical tests, analyzed the data, and drafted the manuscript. All authors read and approved the final manuscript.

Ethics approval

All the procedures were approved by the Research Ethics Committee of Tabriz University of Medical Sciences (reference number: IR.TBZMED.REC.1399.083) and were performed following the approved proposal.

Data availability

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

Declaration of interest

The authors report no conflict of interest.

Additional information

Funding

This article results from a research project (grant ID 64884) that was financing and conducted at Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.