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Originating from China, COVID-19 became the first-ever coronavirus pandemic, wreaking havoc in 218 nations. The lack of a potential treatment exacerbated by the inability of the healthcare infrastructure to contain the viral trajectory led to a worldwide lockdown. The anthropogenic halt presented an unprecedented background to quantify the effect of the anthroposphere on environmental pollution. Consequently, we analyzed the variations in the air (PM10, PM2.5, NO2, SO2) and water pollutants (BOD, COD, DO, coliform) using real-time monitoring data in the majorly hit Indian metropolitan states during the lockdown in contrast to 2019 levels. The overall AQI (air quality index) de-escalated by −31.35%, −34.35%, −32.63%, −29.25% in Delhi, Tamil Nadu, West Bengal, and Karnataka, respectively, from the 2019 levels. The daily concentrations of NO2, PM2.5, and PM10 plunged tremendously. The exact pre-disposing factors responsible for higher COVID-19 transmission in some geographical centers remain elusive. Investigations have corroborated putative links between air pollutants and COVID-19 mortalities. Therefore, we further mapped PM2.5, PM10, NO2, and SO2 to co-relate with COVID-19 infectivity and mortality across the study states. Significant (P < 0.001) positive correlation between COVID-19 transmission was established for all pollutants with maximum co-relation with AQI followed by NO2. River Ganga water in Uttarakhand was deemed "fit for drinking" for the first time in two decades. An aggregate of −71.94, −61.32, and −77.94 decrease in BOD, COD, total coliform levels, and an 11.75 rise in the average DO levels from 2019 data. This study will better assist the future framework of health and environment restoration policies. [ABSTRACT FROM AUTHOR]

Graph: Figure 5 DAMTC facilitates expansion of hematopoietic progenitors in the BM of TBI mice. Representative images of colonies from naïve, DAMTC and TBI + DAMTC mice are shown (cells from ten animals were examined in each group; n = 10). Panels show colonies of hematopoietic progenitors (A) CFU-GM, (B) CFU-GEMM and (C) BFU-E after performing ex-vivo culturing on day 10 post TBI. [Extracted from the article]

Protection of the hematopoietic system from radiation damage, and/or mitigation of hematopoietic injury are the two major strategies for developing medical countermeasure agents (MCM) to combat radiation-induced lethality. In the present study, we investigated the potential of 7, 8-diacetoxy-4-methylthiocoumarin (DAMTC) to ameliorate radiation-induced hematopoietic damage and the associated mortality following total body irradiation (TBI) in C57BL/6 mice. Administration of DAMTC 24 hours post TBI alleviated TBI-induced myelo-suppression and pancytopenia, by augmenting lymphocytes and WBCs in the peripheral blood of mice, while bone marrow (BM) cellularity was restored through enhanced proliferation of the stem cells. It stimulated multi-lineage expansion and differentiation of myeloid progenitors in the BM and induced proliferation of splenic progenitors thereby, facilitating hematopoietic re-population. DAMTC reduced the radiation-induced apoptotic and mitotic death in the hematopoietic compartment. Recruitment of pro-inflammatory M1 macrophages in spleen contributed to the immune-protection linked to the mitigation of hematopoietic injury. Recovery of the hematopoietic compartment correlated well with mitigation of mortality at a lethal dose of 9 Gy, leading to 80% animal survival. Present study establishes the potential of DAMTC to mitigate radiation-induced injury to the hematopoietic system by stimulating the re-population of stem cells from multiple lineages. [ABSTRACT FROM AUTHOR]

Radiation-induced intestinal injury (RIII) constitutes a crucial clinical element of acute radiation syndrome with life-threatening implications posing challenges in devising effective medical countermeasures. Herein, we report the potential of 7, 8-diacetoxy-4-methylthiocoumarin (DAMTC) to mitigate RIII following total-body irradiation (TBI) in C57BL/6 mice and underlying mechanisms. Administration of DAMTC 24 hours post TBI facilitated structural reconstitution and restoration of functional absorption linked to alleviation of radiation-induced apoptotic death of intestinal crypt progenitor/stem (ICPS) and villus stromal cells through induction of Bcl-2 family-mediated anti-apoptotic signalling. Reduction in TBI-induced DNA damage accumulation coupled with inhibition of cell cycle arrest through stimulation of anti-p53- and anti-p21-dependent synergistic signalling protected ICPS cells from radiation injury. Enhanced proliferation of crypt stem cells, induction of anti-oxidant defence, subjugation of TBI-induced lipid peroxidation and phenotypic polarization of intestinal macrophages to anti-inflammatory M2 class underlie amelioration of RIII. Stimulation of multiple mitigative signalling processes by DAMTC appeared to be associated with enhanced protein acetylation, an important regulator of cellular responses to radiation damage. Our findings establish the mitigative potential of DAMTC against RIII by hyper-acetylation-mediated epigenetic regulation, which triggers axes of anti-apoptotic and pro-survival pathways, enabling proliferation and maintenance of ICPS cells leading to epithelial regeneration. [ABSTRACT FROM AUTHOR]