Gratitude for the analysis of advances in the metabolic interactions of fats. Redox equilibrium in oxidation and reduction processes occurs when the overall balance of these chemical reactions remains stable. This is what is observed in normal physiology.
If, on the other hand, the organism becomes unbalanced, the production of ROS accelerates. These molecules accumulate within cells, oxidizing and altering the substances they contain, such as lipids, proteins, and DNA.
Redox equilibrium is essential for cellular homeostasis. Overproduction of ROS and/or depletion of enzymatic and non-enzymatic antioxidant systems can lead to oxidative stress (OS) and its consequences. Excess reducing equivalents can regulate cell signaling pathways, modify transcriptional activity, induce alterations in disulfide bond formation in proteins, reduce mitochondrial function, decrease cellular metabolism, and contribute to the development of some diseases in which NF-κB, a redox agent, participates as a transcription factor. Some of these diseases include protein aggregation cardiomyopathy, hypertrophic cardiomyopathy, muscular dystrophy, pulmonary hypertension, rheumatoid arthritis, Alzheimer's disease, and metabolic syndrome, among others (Table 1 of the first link).
Environmental factors such as sedentary lifestyle, obesity, inadequate diet, smoking, and environmental pollution also contribute to the development of redox imbalance. Cell repair and the antioxidant system work together to counteract the damage caused by ROS. Endogenous redox enzymes are generally enzymes, such as peroxidases and catalases. Reviewed data show that prolonged deviations from this redox state generate oxidative or reducing stress, which is responsible for inflammation, allergic and autoimmune reactions, and also contributes to aging.
Treatment with stearoylethanolamide (SEA) is neuroprotective against LPS-induced neuroinflammation. SEA restricted the spread of peripheral inflammation to the brain and prevented the activation of resident microglia and leukocyte trafficking to the brain parenchyma. SEA improved the amplitude of synaptic vesicle release, supported a balanced signal-to-noise ratio in glutamate and GABAergic neurotransmission, and decreased the excitotoxic risk associated with higher glutamate levels.
Physical exercise stimulates the secretion of irisin, which has been shown to be a potent protector of the aforementioned organs and tissues. Along with melatonin, it can promote redox homeostasis.
Recent publications also show ROS as compounds essentially linked to positive effects on athletes' health. The anti-inflammatory effect associated with exercise, muscle biogenesis through redox-sensitive mechanisms, improved glycogen replenishment, and even increased muscle contractility and strength are some of the positive effects of cellular signaling by ROS.
Mitochondria are essential for providing energy to maintain cell viability. Oxidative phosphorylation involves the transfer of electrons from energy substrates to oxygen to produce adenosine triphosphate (ATP). Mitochondria also regulate cell proliferation, metastasis, and deterioration. Electron flow in the mitochondrial respiratory chain generates reactive oxygen species (ROS), which are harmful to cells at elevated levels. Glutathione (GSH) is an abundant cellular antioxidant that is primarily synthesized in the cytoplasm and delivered to the mitochondria. Mitochondrial oxidative stress and mGSH depletion are implicated in many pathological conditions associated with mitochondrial abnormalities and dysfunctions, as well as with disease and aging. Restoring mGSH levels and the GSH/GSSG ratio, as well as reducing ROS accumulation, are critical for maintaining mitochondrial function and antioxidant defense.
A long-term imbalance in the mitochondrial ROS/mGSH ratio can cause cellular dysfunction, apoptosis, necroptosis, and ferroptosis, which can lead to disease. This study reviews the physiological functions, anabolism, variations in organ tissue accumulation, and delivery of GSH to mitochondria, as well as the relationships between mGSH levels, the GSH/GSH disulfide (GSSG) ratio, programmed cell death, and ferroptosis.
Dietary supplements are associated with higher GSH levels and antioxidant effects, as well as with levels of inflammatory biomarkers. Probiotics can increase GSH levels, thereby reducing inflammation and oxidative stress (Table 2). Ginsenosides affect oxidative stress-related markers such as SOD, MDA, GSH, GSH-P X, and catalase, and reduce levels of inflammatory factors. A systematic review and meta-analysis showed that saffron supplementation can significantly increase TAC and GSH-P X levels, suggesting that saffron may reduce markers of oxidative stress. The main mechanism of the neuroprotective effect of moringa extract and its phytochemical derivatives is to reduce oxidative stress by increasing levels of antioxidant enzymes, reducing TAC levels, and inducing the overproduction of SOD and GSH. Furthermore, a systematic review and meta-analysis showed that chromium supplementation significantly increases GSH levels. The anti-inflammatory and antioxidant properties of zinc may also have broad therapeutic effects in cardiovascular diseases. Zinc supplementation significantly reduced levels of nitric oxide, MDA, TAC, and GSH (Table 3). The second link presents a review exploring the connection between ferroptosis, the NRF2 pathway, and atherosclerosis, emphasizing its role in protecting cells from oxidative stress and maintaining iron balance. The use of iron chelating agents to manage iron overload is analyzed, along with their associated benefits and challenges. Finally, the importance of exploring therapeutic strategies that enhance the glutathione (GSH) system and the potential of natural compounds such as quercetin, terpenoids, and phenolic acids to reduce oxidative stress is highlighted.
Concerned about Mercury in fish - Anti-Fish...Concerned about Vaccine Safety - Anti-Vaxxer...Concerned about LA Oil's - oh no - a new tag line to confuse the public - Anti - Oiler's?
So refreshing to have information, research starting from where it should, at the beginnings of all the many processes. Start at the base, the foundation processes and how they fuel and move on up a chain of interacting systems, to then throughout every life giving organs of humans. What keeps our bodies in healthy, cyclical patterns. Health building, not band aid Pass the Loot for meds to suppress the worst symptoms from what are so many unnecessary Dis-Ease's.
As pointed out in this article, watch for this tactic throughout the whole of Legacy, Mainstream Media, Official Institutions, Sources... [dismiss - fill in the blank for the concern - and frame the entire discussion through a narrow lens of look at this. This one thing and one thing only we want you to focus on - while ignoring no matter how vast the body is of research exposing a much bigger, more important revelation, story.]
Focus on what makes for a healthy Gut, Mitochondrial Foundation to make a healthy body/mind. If we can achieve a Healthy Body, no need to chase losing weight, yoyo diets schemes. Feed the body Real Food in the right proportions and the body adjusts its self to its own proper range. Throw away those bath room scales. The many decades of Yoyo diets are just take it off, then put it back on, wash rinse and repeat. Yoyo diets are just one more Ca$h Cow Treadmill. Yoyo diet schemes deprive a body of the necessary nutrition, nutrients and ultimately most likely lead to Chronic Dis-Ease.
Gratitude for the analysis of advances in the metabolic interactions of fats. Redox equilibrium in oxidation and reduction processes occurs when the overall balance of these chemical reactions remains stable. This is what is observed in normal physiology.
If, on the other hand, the organism becomes unbalanced, the production of ROS accelerates. These molecules accumulate within cells, oxidizing and altering the substances they contain, such as lipids, proteins, and DNA.
Redox equilibrium is essential for cellular homeostasis. Overproduction of ROS and/or depletion of enzymatic and non-enzymatic antioxidant systems can lead to oxidative stress (OS) and its consequences. Excess reducing equivalents can regulate cell signaling pathways, modify transcriptional activity, induce alterations in disulfide bond formation in proteins, reduce mitochondrial function, decrease cellular metabolism, and contribute to the development of some diseases in which NF-κB, a redox agent, participates as a transcription factor. Some of these diseases include protein aggregation cardiomyopathy, hypertrophic cardiomyopathy, muscular dystrophy, pulmonary hypertension, rheumatoid arthritis, Alzheimer's disease, and metabolic syndrome, among others (Table 1 of the first link).
Environmental factors such as sedentary lifestyle, obesity, inadequate diet, smoking, and environmental pollution also contribute to the development of redox imbalance. Cell repair and the antioxidant system work together to counteract the damage caused by ROS. Endogenous redox enzymes are generally enzymes, such as peroxidases and catalases. Reviewed data show that prolonged deviations from this redox state generate oxidative or reducing stress, which is responsible for inflammation, allergic and autoimmune reactions, and also contributes to aging.
Treatment with stearoylethanolamide (SEA) is neuroprotective against LPS-induced neuroinflammation. SEA restricted the spread of peripheral inflammation to the brain and prevented the activation of resident microglia and leukocyte trafficking to the brain parenchyma. SEA improved the amplitude of synaptic vesicle release, supported a balanced signal-to-noise ratio in glutamate and GABAergic neurotransmission, and decreased the excitotoxic risk associated with higher glutamate levels.
Physical exercise stimulates the secretion of irisin, which has been shown to be a potent protector of the aforementioned organs and tissues. Along with melatonin, it can promote redox homeostasis.
Recent publications also show ROS as compounds essentially linked to positive effects on athletes' health. The anti-inflammatory effect associated with exercise, muscle biogenesis through redox-sensitive mechanisms, improved glycogen replenishment, and even increased muscle contractility and strength are some of the positive effects of cellular signaling by ROS.
https://www.mdpi.com/2076-3921/12/5/1126 (2023).--
https://www.sciencedirect.com/science/article/pii/S1568163723001150 (2023).--
https://www.sciencedirect.com/science/article/abs/pii/S2212429223000111 (2023).--
https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00012-8 (2023).—
https://link.springer.com/article/10.1007/s00204-023-03562-9 (2023).--
https://www.liebertpub.com/doi/full/10.1089/ars.2019.7803 (2020).--
https://pubmed.ncbi.nlm.nih.gov/31881191/ (2020).--
https://www.sciencedirect.com/science/article/abs/pii/S0065230X21000336 (2021).--
https://www.tandfonline.com/doi/full/10.1080/19396368.2022.2119181 (2022).--
Mitochondria are essential for providing energy to maintain cell viability. Oxidative phosphorylation involves the transfer of electrons from energy substrates to oxygen to produce adenosine triphosphate (ATP). Mitochondria also regulate cell proliferation, metastasis, and deterioration. Electron flow in the mitochondrial respiratory chain generates reactive oxygen species (ROS), which are harmful to cells at elevated levels. Glutathione (GSH) is an abundant cellular antioxidant that is primarily synthesized in the cytoplasm and delivered to the mitochondria. Mitochondrial oxidative stress and mGSH depletion are implicated in many pathological conditions associated with mitochondrial abnormalities and dysfunctions, as well as with disease and aging. Restoring mGSH levels and the GSH/GSSG ratio, as well as reducing ROS accumulation, are critical for maintaining mitochondrial function and antioxidant defense.
A long-term imbalance in the mitochondrial ROS/mGSH ratio can cause cellular dysfunction, apoptosis, necroptosis, and ferroptosis, which can lead to disease. This study reviews the physiological functions, anabolism, variations in organ tissue accumulation, and delivery of GSH to mitochondria, as well as the relationships between mGSH levels, the GSH/GSH disulfide (GSSG) ratio, programmed cell death, and ferroptosis.
Dietary supplements are associated with higher GSH levels and antioxidant effects, as well as with levels of inflammatory biomarkers. Probiotics can increase GSH levels, thereby reducing inflammation and oxidative stress (Table 2). Ginsenosides affect oxidative stress-related markers such as SOD, MDA, GSH, GSH-P X, and catalase, and reduce levels of inflammatory factors. A systematic review and meta-analysis showed that saffron supplementation can significantly increase TAC and GSH-P X levels, suggesting that saffron may reduce markers of oxidative stress. The main mechanism of the neuroprotective effect of moringa extract and its phytochemical derivatives is to reduce oxidative stress by increasing levels of antioxidant enzymes, reducing TAC levels, and inducing the overproduction of SOD and GSH. Furthermore, a systematic review and meta-analysis showed that chromium supplementation significantly increases GSH levels. The anti-inflammatory and antioxidant properties of zinc may also have broad therapeutic effects in cardiovascular diseases. Zinc supplementation significantly reduced levels of nitric oxide, MDA, TAC, and GSH (Table 3). The second link presents a review exploring the connection between ferroptosis, the NRF2 pathway, and atherosclerosis, emphasizing its role in protecting cells from oxidative stress and maintaining iron balance. The use of iron chelating agents to manage iron overload is analyzed, along with their associated benefits and challenges. Finally, the importance of exploring therapeutic strategies that enhance the glutathione (GSH) system and the potential of natural compounds such as quercetin, terpenoids, and phenolic acids to reduce oxidative stress is highlighted.
https://www.mdpi.com/1422-0067/25/2/1314 (2024).--
https://www.mdpi.com/2227-9059/12/3/558 (2024).--
Concerned about Mercury in fish - Anti-Fish...Concerned about Vaccine Safety - Anti-Vaxxer...Concerned about LA Oil's - oh no - a new tag line to confuse the public - Anti - Oiler's?
So refreshing to have information, research starting from where it should, at the beginnings of all the many processes. Start at the base, the foundation processes and how they fuel and move on up a chain of interacting systems, to then throughout every life giving organs of humans. What keeps our bodies in healthy, cyclical patterns. Health building, not band aid Pass the Loot for meds to suppress the worst symptoms from what are so many unnecessary Dis-Ease's.
As pointed out in this article, watch for this tactic throughout the whole of Legacy, Mainstream Media, Official Institutions, Sources... [dismiss - fill in the blank for the concern - and frame the entire discussion through a narrow lens of look at this. This one thing and one thing only we want you to focus on - while ignoring no matter how vast the body is of research exposing a much bigger, more important revelation, story.]
Focus on what makes for a healthy Gut, Mitochondrial Foundation to make a healthy body/mind. If we can achieve a Healthy Body, no need to chase losing weight, yoyo diets schemes. Feed the body Real Food in the right proportions and the body adjusts its self to its own proper range. Throw away those bath room scales. The many decades of Yoyo diets are just take it off, then put it back on, wash rinse and repeat. Yoyo diets are just one more Ca$h Cow Treadmill. Yoyo diet schemes deprive a body of the necessary nutrition, nutrients and ultimately most likely lead to Chronic Dis-Ease.
CHICKEN BREAST, IS ONLY AROUND 1 GRAM FAT, PER 100 GM SERVING, LEAN PORK MINCE, AROUND 3 GM...
SURELY THESE ARE SAFE TO EAT , WITHIN YOUR GUIDELINES ??
( THEIR CONDITIONS ARE ANOTHER MATTER, ENTIRELY, BUT I'M ON A BUDGET...)