Mitigation of the replication of SARS-CoV-2 by Nitric Oxide in Vitro
Published in Redox Biology
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Do free radical NETwork and oxidative stress disparities in African Americans enhance their vulnerability to SARS-CoV-2 ...
Published in Redox biology
This review focuses on the hypothetical mechanisms for enhanced vulnerability of African Americans to SARS-CoV-2 infection, COVID-19 severity, and increased deaths. A disproportionately higher number of African Americans are afflicted with autoimmune and inflammatory diseases (e.g., diabetes, hypertension, obesity), and SARS-CoV-2 has helped expose...
Selenium and selenoproteins in viral infection with potential relevance to COVID-19
Published in Redox Biology
• Many RNA (or reverse transcribing) viruses are more pathogenic in Se deficient hosts. • Both as dietary factor and pharmacological agent, Se can protect against some viruses. • Various selenoproteins contribute to host immunity & play roles in viral pathogenesis. • Se adequacy can prevent excessive cytokine activation and enhance adaptive immunit...
Activation of NRF2 by topical apocarotenoid treatment mitigates radiation-induced dermatitis
Published in Redox Biology
• The apocarotenoid bixin prevents IR-induced damage via the NRF2 signaling pathway. • Topical application of bixin prevents radiation-induced dermatitis in vivo. • NRF2 is a critical mediator of bixin protection against IR-induced cutaneous damage. • Glutathione upregulation contributes to bixin protection against IR-induced ROS and genotoxic stre...
Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.
Published in Redox biology
The autophagic pathway involves the encapsulation of substrates in double-membraned vesicles, which are subsequently delivered to the lysosome for enzymatic degradation and recycling of metabolic precursors. Autophagy is a major cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelle...
Generation and characterization of keap1a- and keap1b-knockout zebrafish.
Published in Redox biology
The Keap1-Nrf2 pathway is an evolutionarily conserved mechanism that protects cells from oxidative stress and electrophiles. Under homeostatic conditions, Keap1 interacts with Nrf2 and leads to its rapid proteasomal degradation, but when cells are exposed to oxidative stress/electrophiles, Keap1 senses them, resulting in an improper Keap1-Nrf2 inte...
Increases of iASPP-Keap1 interaction mediated by syringin enhance synaptic plasticity and rescue cognitive impairments v...
Published in Redox biology
Oxidative stress is an important pathogenic manifestation of Alzheimer's disease (AD) that contributes to synaptic dysfunction, which precedes Aβ accumulation and neurofibrillary tangle formation. However, the molecular machineries that govern the decline of antioxidative defence in AD remains to be elucidated, and effective candidate for AD treatm...
Interrelation between ROS and Ca2+ in aging and age-related diseases.
Published in Redox biology
Calcium (Ca2+) and reactive oxygen species (ROS) are versatile signaling molecules coordinating physiological and pathophysiological processes. While channels and pumps shuttle Ca2+ ions between extracellular space, cytosol and cellular compartments, short-lived and highly reactive ROS are constantly generated by various production sites within the...
The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage.
Published in Redox biology
High-intensity exercise damages mitochondrial DNA (mtDNA) in skeletal muscle. Whether MitoQ - a redox active mitochondrial targeted quinone - can reduce exercise-induced mtDNA damage is unknown. In a double-blind, randomized, placebo-controlled design, twenty-four healthy male participants consisting of two groups (placebo; n = 12, MitoQ; n = 12) p...
Formononetin ameliorates oxaliplatin-induced peripheral neuropathy via the KEAP1-NRF2-GSTP1 axis.
...Published in Redox biology
Management of oxaliplatin-induced peripheral neuropathy (OIPN) has proven challenging owing to the concern that any OIPN-preventing agents may also decrease the efficacy of the chemotherapeutic agent and fail to reverse established neuronal damage. Nevertheless, targeting redox signaling pathways constitutes a promising therapy in OIPN and we have ...
