IDEAS home Printed from https://ideas.repec.org/a/gam/jijerp/v16y2019i13p2389-d245963.html
   My bibliography  Save this article

Morin Protects Human Respiratory Cells from PM 2.5 Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression

Author

Listed:
  • Indhumathi Veerappan

    (Department of Biotechnology, Anna University, BIT Campus, Tiruchirappalli 620 024, India)

  • Senthil Kumar Sankareswaran

    (Department of Biotechnology, Anna University, BIT Campus, Tiruchirappalli 620 024, India)

  • Rajaguru Palanisamy

    (Department of Biotechnology, Anna University, BIT Campus, Tiruchirappalli 620 024, India)

Abstract

Chronic fine particulate matter (PM 2.5 ) exposure causes oxidative stress and leads to many diseases in human like respiratory and cardiovascular disorders, and lung cancer. It is known that toxic responses elicited by PM 2.5 particles depend on its physical and chemical characteristics that are greatly influenced by the source. Dietary polyphenolic compounds that possess antioxidant and free radical scavenging properties could be used for therapeutic or preventive approaches against air pollution related health hazards. This study evaluates characteristics and toxicity of PM 2.5 collected from rural, urban, industrial, and traffic regions in and around Coimbatore City, Tamilnadu, India. Traffic PM 2.5 particles contained higher amounts of metals and polycyclic aromatic hydrocarbons (PAHs). It also possessed higher levels of oxidative potential, induced more intracellular reactive oxygen species (ROS), and caused more levels of cell death and DNA damage in human respiratory cells. Its exposure up regulated DNA damage response related miR222, miR210, miR101, miR34a, and miR93 and MycN and suppressed Rad52. Pre-treatment with morin significantly decreased the PM 2.5 induced toxicity and conferred protection against PM 2.5 induced altered miRNA expression. Results of this study showed that cytoprotective effect of morin is due to its antioxidative and free radical scavenging activity.

Suggested Citation

  • Indhumathi Veerappan & Senthil Kumar Sankareswaran & Rajaguru Palanisamy, 2019. "Morin Protects Human Respiratory Cells from PM 2.5 Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression," IJERPH, MDPI, vol. 16(13), pages 1-20, July.
  • Handle: RePEc:gam:jijerp:v:16:y:2019:i:13:p:2389-:d:245963
    as

    Download full text from publisher

    File URL: https://www.mdpi.com/1660-4601/16/13/2389/pdf
    Download Restriction: no

    File URL: https://www.mdpi.com/1660-4601/16/13/2389/
    Download Restriction: no
    ---><---

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:gam:jijerp:v:16:y:2019:i:13:p:2389-:d:245963. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: MDPI Indexing Manager (email available below). General contact details of provider: https://www.mdpi.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.