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The Beneficial Effects of QIAPI 1((R)) against Pentavalent Arsenic-Induced Lung Toxicity: A Hypothetical Model for SARS CoV2-I nduced Lung Toxicity #MMPMID33845734
Herrera AS; Beeraka NM; Sinelnikov MY; Nikolenko VN; Giller DB; Solis LFT; Mikhaleva LM; Somasundaram SG; Kirkland CE; Aliev G
Curr Pharm Biotechnol 2022[]; 23 (2): 307-315 PMID33845734show ga
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((R)), 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 commonalitie of lung pathology of SARS CoV and As-induced toxicity, the aim of this study is to decipher the efficacy of QIAPI 1((R)) 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((R)). 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((R)) significantly associated with mitigated histological signs of lung inflammation induced by Arsenic. Therefore, QIAPI 1((R)) 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((R)) in SARS CoV2-induced pulmonary damage. Future studies are warranted to delineate the efficacy of QIAPI 1(R) against SARS CoV and SARS CoV2 lung pathology.