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. 2021 Nov 25;142:106946. doi: 10.1016/j.vph.2021.106946

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© 2021 Published by Elsevier Inc.

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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Fig. 3 — SARS-CoV-2 increases mitochondrial dysfunction.

Fluorescence intensity depicting (A and B) mitochondrial ROS (MitoSOX Red®) and (C and D) mitochondrial potential (MitoTracker® Red CMXRos, FlexStation-3) in control (MOCK and UV-inactivated SARS-CoV-2-exposed HUVECs) and SARS-CoV-2-infected (MOI 2–24 or 48 h) HUVECs. Rotenone and FCCP were used as positive controls. Acridine orange (green) and DAPI (blue) were utilized for the nucleus staining. Immunoblot representative imagens (bottom) and densitometric analysis (top) of protein levels of (E) mitochondrial complex I and (F) VDAC (voltage-dependent ion channel) normalized by β-actin in MOCK and SARS-CoV-2-infected HUVECs. The results are expressed as the mean ± SEM. Statistical significance was determined by one-way ANOVA multiple comparations with Tukey post-hoc test or t-test when appropriated (n = 5–6), using the Prism GraphPad 8.0 software. Statistically significant differences were considered when p < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)