Melanin (https://www.ncbi.nlm.nih.gov/books/NBK459156/) is the main pigment responsible for skin, hair, and eye color. Melanin biosynthesis is primarily mediated by the enzyme tyrosinase (https://www.ncbi.nlm.nih.gov/books/NBK459156/). Inhibitors of this enzyme can be used to lighten the skin, eyes, and hair, but acetylsalicylic acid does not inhibit the direct catalytic activity of tyrosinase, so it is not an inhibitor. It directly inhibits the expression of tyrosinase (https://www.semanticscholar.org/pap...ashi/76c261e7bcbe1511a8178601e115d43144542597).
Acetylsalicylic acid (aspirin; ASA) is widely used as an analgesic/antipyretic drug. ASA exhibits a wide range of biological effects, including preventive effects against heart attack, stroke, and the development of some types of cancer. However, the effects of ASA on melanogenesis are not well known. Therefore, we investigated the effect of ASA on melanin production using B16 murine melanoma cells and demonstrated a new biological effect of ASA. In the presence of alpha-melanocyte stimulating hormone (alpha-MSH), B16 melanoma cells are stimulated to enhance melanin synthesis. ASA (2 mM) inhibited alpha-MSH-enhanced melanin synthesis in melanoma more strongly than other well-known anti-melanogenic agents such as arbutin (2 mM) and kojic acid (200 microM). Interestingly, ASA did not inhibit the catalytic activity of mushroom tyrosinase (concentration range 0.5-4.0 mM). To clarify the target of ASA action in melanogenesis, we performed Western blotting for tyrosinase, which is a key melanogenic enzyme. ASA inhibited tyrosinase expression in a dose-dependent manner. Therefore, the depigmenting effect of ASA might be due to inhibition of tyrosinase expression or enhancement of tyrosinase degradation. This study suggests that ASA is a candidate anti-melanogenic agent and it might be effective in hyperpigmentation disorders.
THE EFFECT OF ASPIRIN ON FAT BURN
The action of the strongest fat burners is based on the effect on dissociating proteins. Fat burners of this class allow you to lose 10 kg or more per month.
Mitochondrial anion transporter proteins that function as dimers and form proton channels in the inner mitochondrial membrane, which creates proton leakage and decouples oxidative phosphorylation from ATP synthesis, resulting in the release of heat instead of ATP.
In short, instead of converting energy for body function, the energy is converted into pure heat. The fat literally burns.
Substances that affect the uncoupling proteins in this way are called uncoupling agents.
Aspirin is no exception.
Stadi1
Gluconeogenesis, glycolysis and glycogenolysis were studied in perfused rat liver after infusion of different concentrations of diclofenac and aspirin, two non-steroidal anti-inflammatory drugs (NSAIDs). Glucose synthesis was measured in the liver of rats given a Krebs-Henseleit bicarbonate buffer containing l-lactate (2 mm) and pyruvate (0.1 mm) as precursors for 48 hours on an empty stomach. Both diclofenac (0.01-0.1 mm) and aspirin (1-10 mm) had an inhibitory effect on gluconeogenesis (GNG). The inhibition was dose-dependent and reversible. (https://www.sciencedirect.com/science/article/pii/S0005272896001090)
Stadi2
It is known that salicylic acid causes a disruption in the activity of mitochondrial oxidative phosphorylation; however, the observed inhibition of octanoic acid oxidation by salicylic acid is not due to a deficiency of ATP, since the enzyme activity was measured in the presence of 10 mM exogenously added ATP. These studies clearly demonstrate that salicylic acid inhibits fatty acid oxidation in mitochondria, but does not affect fatty acid oxidation in peroxisomes. (https://www.nature.com/articles/pr1988269.pdf)
In conclusion, it is worth noting that the dosages required for this are toxic to the liver and kidneys, deplete electrolytes, cause nausea and vomiting, lead to internal bleeding, and can even result in death.
Therefore, this post is more of a fanfiction. It is intended for general knowledge.
TG @OGR_IZ_DNR
Acetylsalicylic acid (aspirin; ASA) is widely used as an analgesic/antipyretic drug. ASA exhibits a wide range of biological effects, including preventive effects against heart attack, stroke, and the development of some types of cancer. However, the effects of ASA on melanogenesis are not well known. Therefore, we investigated the effect of ASA on melanin production using B16 murine melanoma cells and demonstrated a new biological effect of ASA. In the presence of alpha-melanocyte stimulating hormone (alpha-MSH), B16 melanoma cells are stimulated to enhance melanin synthesis. ASA (2 mM) inhibited alpha-MSH-enhanced melanin synthesis in melanoma more strongly than other well-known anti-melanogenic agents such as arbutin (2 mM) and kojic acid (200 microM). Interestingly, ASA did not inhibit the catalytic activity of mushroom tyrosinase (concentration range 0.5-4.0 mM). To clarify the target of ASA action in melanogenesis, we performed Western blotting for tyrosinase, which is a key melanogenic enzyme. ASA inhibited tyrosinase expression in a dose-dependent manner. Therefore, the depigmenting effect of ASA might be due to inhibition of tyrosinase expression or enhancement of tyrosinase degradation. This study suggests that ASA is a candidate anti-melanogenic agent and it might be effective in hyperpigmentation disorders.
THE EFFECT OF ASPIRIN ON FAT BURN
The action of the strongest fat burners is based on the effect on dissociating proteins. Fat burners of this class allow you to lose 10 kg or more per month.
Mitochondrial anion transporter proteins that function as dimers and form proton channels in the inner mitochondrial membrane, which creates proton leakage and decouples oxidative phosphorylation from ATP synthesis, resulting in the release of heat instead of ATP.
In short, instead of converting energy for body function, the energy is converted into pure heat. The fat literally burns.
Substances that affect the uncoupling proteins in this way are called uncoupling agents.
Aspirin is no exception.
Stadi1
Gluconeogenesis, glycolysis and glycogenolysis were studied in perfused rat liver after infusion of different concentrations of diclofenac and aspirin, two non-steroidal anti-inflammatory drugs (NSAIDs). Glucose synthesis was measured in the liver of rats given a Krebs-Henseleit bicarbonate buffer containing l-lactate (2 mm) and pyruvate (0.1 mm) as precursors for 48 hours on an empty stomach. Both diclofenac (0.01-0.1 mm) and aspirin (1-10 mm) had an inhibitory effect on gluconeogenesis (GNG). The inhibition was dose-dependent and reversible. (https://www.sciencedirect.com/science/article/pii/S0005272896001090)
Stadi2
It is known that salicylic acid causes a disruption in the activity of mitochondrial oxidative phosphorylation; however, the observed inhibition of octanoic acid oxidation by salicylic acid is not due to a deficiency of ATP, since the enzyme activity was measured in the presence of 10 mM exogenously added ATP. These studies clearly demonstrate that salicylic acid inhibits fatty acid oxidation in mitochondria, but does not affect fatty acid oxidation in peroxisomes. (https://www.nature.com/articles/pr1988269.pdf)
In conclusion, it is worth noting that the dosages required for this are toxic to the liver and kidneys, deplete electrolytes, cause nausea and vomiting, lead to internal bleeding, and can even result in death.
Therefore, this post is more of a fanfiction. It is intended for general knowledge.
TG @OGR_IZ_DNR
