Title:The Beneficial Effects of QIAPI 1® against Pentavalent Arsenic-Induced
Lung Toxicity: A Hypothetical Model for SARS CoV2-I nduced Lung
Toxicity
Volume: 23
Issue: 2
Author(s): Arturo Solís Herrera, Narasimha M. Beeraka, Mikhail Y. Sinelnikov, Vladimir N. Nikolenko, Dimitry B. Giller, Luis Fernando Torres Solis, Liudmila M. Mikhaleva, Siva G. Somasundaram*, Cecil E. Kirkland and Gjumrakch Aliev
Affiliation:
- Department of Biological Sciences, Salem University,
Salem, WV, USA
Keywords:
COVID-19, SARS-CoV2, QIAPI1®, alveoli, arsenic, lung toxicity, fibrosis.
Abstract: Exposure to environmental toxicants such as Arsenic (As) can result in As-induced alterations
in immune regulators. Consequently, people who are more prone to viral infections like influenza A or
B, H1N1, SARS CoV (Severe Acute Respiratory Syndrome Coronavirus), and SARS CoV2 may develop
a susceptibility to immune responses in their lungs because our previous reports delineated the ability
of QIAPI 1®, a melanin precursor, to dissociate water molecules with simultaneous therapeutic efficacy
against central nervous system (CNS) diseases, retinopathy, and As-induced renal toxicity. Considering
the commonalities of lung pathology of SARS CoV and As-induced toxicity, the aim of this study is to
decipher the efficacy of QIAPI 1® against pentavalent As-induced lung toxicity by examining the pulmonary
pathology. Hematoxylin & Eosin (H&E) staining was used for ascertaining the lung pathology
in Wistar rat models. Animals were divided into 3 groups: control group, group treated with pentavalent
As, and a group treated with pentavalent As and QIAPI 1®. There were no significant changes in lung
histopathology in the control group as indicated by intact morphology. The As-treated group revealed
damage to the histoarchitecture with pulmonary edema, interstitial fibrosis, diffuse alveolar damage,
Bronchiolitis obliterans organizing pneumonia (BOOP)-lesions, formation of hyaline membrane, multinucleated
giant pneumocytes, atypical pneumocytes, inflammatory cell infiltration, and interstitial edema.
The group treated with As and QIAPI 1® significantly associated with mitigated histological signs of
lung inflammation induced by Arsenic. Therefore, QIAPI 1® can be recommended as antagonistic to Asinduced
lung toxicity. In conclusion, this model could be preferred as a hypothetical model to examine
the efficacy of QIAPI 1® in SARS CoV2-induced pulmonary damage. Future studies are warranted to
delineate the efficacy of QIAPI 1® against SARS CoV and SARS CoV2 lung pathology.
