A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients
Joint Authors
Abd al-Rahman, Fatimah G.
al-Bindari, Riham N.
al-Harbi, Fadiyah Ahmad
al-Hamrani, Sultan Qalit
Mégarbane, Bruno
Source
Saudi Journal of Biological Sciences
Issue
Vol. 28, Issue 6 (30 Jun. 2021), pp.3540-3547, 8 p.
Publisher
Publication Date
2021-06-30
Country of Publication
Saudi Arabia
No. of Pages
8
Main Subjects
Abstract EN
Hypozincemia is prevalent in severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)-infected patients and has been considered as a risk factor in severe coronavirus disease-2019 (COVID-19).
Whereas zinc might affect SARS-COV-2 replication and cell entry, the link between zinc deficiency and COVID-19 severity could also be attributed to the effects of COVID-19 on the body metabolism and immune response.
Zinc deficiency is more prevalent in the elderly and patients with underlying chronic diseases, with established deleterious consequences such as the increased risk of respiratory infection.
We reviewed the expected effects of zinc deficiency on COVID-19-related pathophysiological mechanisms focusing on both the renin–angiotensin and kinin-kallikrein systems.
Mechanisms and effects were extrapolated from the available scientific literature.
Zinc deficiency alters angiotensin-converting enzyme-2 (ACE2) function, leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lysdes- Arg9-bradykinin, which results in an exaggerated pro-inflammatory response, vasoconstriction and pro-thrombotic effects.
Additionally, zinc deficiency blocks the activation of the plasma contact system, a protease cascade initiated by factor VII activation.
Suggested mechanisms include the inhibition of Factor XII activation and limitation of high-molecular-weight kininogen, prekallikrein and Factor XII to bind to endothelial cells.
The subsequent accumulation of Factor XII and deficiency in bradykinin are responsible for increased production of inflammatory mediators and marked hypercoagulability, as typically observed in COVID-19 patients.
To conclude, zinc deficiency may affect both the renin–angiotensin and kinin-kallikrein systems, leading to the exaggerated inflammatory manifestations characteristic of severe COVID-19.
American Psychological Association (APA)
Jawdah, Ahmad S.& Abd al-Rahman, Fatimah G.& al-Bindari, Riham N.& al-Harbi, Fadiyah Ahmad& al-Hamrani, Sultan Qalit& Mégarbane, Bruno. 2021. A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients. Saudi Journal of Biological Sciences،Vol. 28, no. 6, pp.3540-3547.
https://search.emarefa.net/detail/BIM-1431467
Modern Language Association (MLA)
Jawdah, Ahmad S.…[et al.]. A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients. Saudi Journal of Biological Sciences Vol. 28, no. 6 (2021), pp.3540-3547.
https://search.emarefa.net/detail/BIM-1431467
American Medical Association (AMA)
Jawdah, Ahmad S.& Abd al-Rahman, Fatimah G.& al-Bindari, Riham N.& al-Harbi, Fadiyah Ahmad& al-Hamrani, Sultan Qalit& Mégarbane, Bruno. A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients. Saudi Journal of Biological Sciences. 2021. Vol. 28, no. 6, pp.3540-3547.
https://search.emarefa.net/detail/BIM-1431467
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references : p. 3545-3547
Record ID
BIM-1431467