I did not have lung congestion - it was more like collapse of cellular and metabolic function...
From AI:
N-Acetylcysteine (NAC) can help restore cellular homeostasis in a number of ways:
Glutathione (GSH) levels NAC is a precursor to GSH synthesis, and can help restore GSH levels that have been depleted. GSH is a key endogenous thiol antioxidant that can be depleted during oxidative stress. Restoring GSH levels can help prevent apoptosis caused by GSH depletion.
Redox homeostasis NAC can help restore redox homeostasis that has been disrupted by viral infections, such as SARS-CoV-2, which overproduces reactive oxygen species (ROS).
Protein quality control Loss of NAC can activate the ER stress response, which can lead to cell death. NAC plays a crucial role in protein quality control and maintaining cellular homeostasis.
MDPI Mitochondrial Glutathione in Cellular Redox Homeostasis and ... NAC supplementation may restore cellular GSH levels and prevent apoptosis caused by GSH de...
Nature Naca protects the larval fat body from cell death by ... - Nature Sep 1, 2023 — In several species and cell lines, the loss of NAC activates the ER stress resp...
NCBI N-Acetyl Cysteine Restores the Diminished Activity of ... - NCBI Apr 14, 2023 — SARS-CoV-2 infects type II pneumocytes and disrupts redox homeostasis by overp...
IOVS N-Acetylcysteine Amide Protects Against Oxidative Stress ...
... NAC.73–76 One of the key endogenous thiol antioxidants is GSH, which is depleted durin... NAC has also been used to treat other conditions, including:
Respiratory diseases NAC supplementation can help replenish GSH levels in patients with respiratory diseases, and may also help with pulmonary recovery.
COPD NAC has been shown to attenuate lung damage, emphysema, and alveolar septal cell apoptosis in rats with cigarette smoke-induced COPD.
NAC has antioxidant and anti-inflammatory properties, and has been used as an over-the-counter nutritional supplement in the United States, Canada, and Australia for decades. However, continuous NAC treatment beyond the injury phase can delay regeneration by impairing mitochondrial biogenesis. This is for informational purposes only. For medical advice or diagnosis, consult a professional. Generative AI is experimental.
N-acetylcysteine (NAC) comes from the amino acid L-cysteine and has been a Food and Drug Administration (FDA) approved drug since 1963. It is recognized as the standard treatment for acetaminophen overdose and has been used as a mucolytic drug since the 1960s [1]. NAC has also been used as a supplement for decades and, as such, can be found as an over-the-counter nutritional supplement in countries such as the United States, Canada, and Australia [1]. Therefore, NAC falls into a grey zone with other compounds such as cannabidiol (CBD), but as of August 2022, the FDA has backed away from its hard stance on classifying NAC as a drug and is allowing its sale as a dietary supplement [2]. NAC’s antioxidant and anti-inflammatory properties make it a promising therapeutic agent for conditions in which oxidative stress is involved [1]. Examples of these disorders include diabetes, obesity, cancer, neurological disorders, hypertension, pulmonary, inflammatory bowel, cardiovascular, autoimmune, and infectious diseases in humans, as well as domesticated animal weaning disorders, respiratory disease, diarrhea, endometritis, and mastitis [3,4,5,6,7,8,9,10]. While there has been an increasing interest in the use of NAC for a wide range of pathological conditions over the past few decades, various human clinical studies have reported conflicting results, and many other studies were performed in vitro. Therefore, more clinical studies are required to address these conflicting results and to support the purported therapeutic roles of NAC in treating different pathological conditions. Various animal studies involving the use of NAC have also been performed, especially with its use in treating intestinal inflammation and related disorders that can be caused by anti-nutritional factors (e.g., ß-conglycinin, a vicilin storage protein of soybeans), the process of weaning, and consumption of mycotoxins [10,11,12]. Many studies have shown the protective effects of NAC for neonatal animals immune challenged with bacterial lipopolysaccharide (LPS) endotoxin, particularly studies involving piglets [13,14]. NAC administration has consistently been shown to increase daily body weight gain and alleviate LPS-mediated growth depression. Furthermore, the porcine model of ulcerative colitis (UC) can be used to support NAC usage for humans. For example, in a study conducted by Wang et al. (2013), the piglet model of UC demonstrated that administration of NAC was able to reduce colon histopathology score and ameliorate UC histological abnormalities [15]. Despite the numerous NAC studies and its increasing popularity, the mechanisms of action (MOA) by which NAC exerts its antioxidant and cytoprotective properties remain unclear [1,16]. It is often assumed that the effects conferred by NAC are due to it acting as a scavenger of reactive oxygen species (ROS), a precursor for glutathione (GSH) biosynthesis, and a disulfide reductant [16,17]. However, these three major narratives can only explain the effects of NAC under specific circumstances [16,17]. Recently, an alternative MOA was proposed that may explain the effects attributed to NAC: the conversion of NAC into hydrogen sulfide and sulfane sulfur species, which are known to possess antioxidant and cytoprotectant properties [16,17]. Thus, the purpose of this review is to provide an overview of the therapeutic uses of NAC in both humans and domesticated species, with a particular focus on weaning disorders, as well as an overview of its MOA.
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