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why not?
-
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Bezoekers in dit topic
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raad het verder ook niemand aan na eigen ervaringen, maar het kan net zoals clen/t3/eca een ondersteuning zijn op je dieet/cardio mits je de eventuele risico's accepteert van het middel.Gele spermaen t feit dat het een dodelijk goedje is
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In tegenstelling tot al die middelen is DNP altijd toxisch.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550200/
Potential Mechanisms of Toxicity
The classic symptom complex observed by overdose of phenol-based products such as DNP is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea [4, 21, 22]. There are thought to be several physiological mechanisms involved in the development of toxicity of DNP, which are summarised below.
Uncoupling of Oxidative Phosphorylation
DNP decreases the formation of high-energy phosphate bonds in mitochondria and at the same time stimulates systemic oxygen consumption [23]. This dissociative effect is known as uncoupling of oxidative phosphorylation. Adenosine triphosphate (ATP) production is the final product of the tricarboxylic acid (Krebs) cycle in mitocondria along with CO2 and H2O. During glycolysis, there is a net production of two ATP molecules, but the majority of energy-rich phosphate bonds (38 in total) are produced during the final oxidative phosphorylation process. During this final phase, ATP synthetase converts adenosinediphosphate to ATP with the addition of an inorganic phosphate molecule. DNP interferes with the final energy production pathway by preventing the uptake of inorganic phosphate molecules into the mitochondria [24, 25]. This results in the inhibition of all energy-requiring processes and the extra-mitochondrial accumulation of inorganic phosphate [26]. DNP also acts as a chemical ionophore, stopping the final energy conversion by exporting the proton ions (H+) needed for ATP production across the mitochondrial membrane by increasing the basal leak of protons [12]. This shift in the proton electrochemical gradient then results in potential energy dissipating as heat, instead of being converted to ATP, with rapid consumption of calories [27, 28]. The heat production represents a failure in thermoregulatory homeostasis, leading to uncontrolled hyperthermia [29].
Stimulation of Glycolysis
El-Guindy et al. concluded that dinitrophenol produces its glycolytic effect through its effect on the muscle contraction process [30]. Carbohydrate consumption markedly increases in the presence of dinitrophenol which allows for rapid weight loss when dinitrophenol is taken in small doses [26]. Pyruvic acid is aerobically metabolised to H2O and CO2, but results in the production of lactic acid when metabolised anaerobically. The discrepancy between the stimulation of glycolysis and the inhibition of oxidative phosphorylation results in a rapid rise in the production of pyruvic acid, leading to an increased production of lactic acid [24, 26, 31].
Potassium and Phosphate Accumulation
Mudge showed that potassium accumulates in rabbit kidney slices as the concentration of dinitrophenol is increased [32]. The accumulation of potassium continues even after cellular respiration is inhibited [32] and hyperkalaemia has contributed to toxicity [33]. Due to the uncoupling of oxidative phosphorylation, inorganic phosphate is no longer absorbed into the mitochondria and accumulation takes place, but whether this contributes to the clinical presentation is unknown [25, 34].
Teratogenicity, Carcinogenicity and Other Toxicity
In animal studies, DNP has been shown to be teratogenic, mutagenic and carcinogenic; developmental and reproductive toxicity has also been reported [35].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550200/
Potential Mechanisms of Toxicity
The classic symptom complex observed by overdose of phenol-based products such as DNP is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea [4, 21, 22]. There are thought to be several physiological mechanisms involved in the development of toxicity of DNP, which are summarised below.
Uncoupling of Oxidative Phosphorylation
DNP decreases the formation of high-energy phosphate bonds in mitochondria and at the same time stimulates systemic oxygen consumption [23]. This dissociative effect is known as uncoupling of oxidative phosphorylation. Adenosine triphosphate (ATP) production is the final product of the tricarboxylic acid (Krebs) cycle in mitocondria along with CO2 and H2O. During glycolysis, there is a net production of two ATP molecules, but the majority of energy-rich phosphate bonds (38 in total) are produced during the final oxidative phosphorylation process. During this final phase, ATP synthetase converts adenosinediphosphate to ATP with the addition of an inorganic phosphate molecule. DNP interferes with the final energy production pathway by preventing the uptake of inorganic phosphate molecules into the mitochondria [24, 25]. This results in the inhibition of all energy-requiring processes and the extra-mitochondrial accumulation of inorganic phosphate [26]. DNP also acts as a chemical ionophore, stopping the final energy conversion by exporting the proton ions (H+) needed for ATP production across the mitochondrial membrane by increasing the basal leak of protons [12]. This shift in the proton electrochemical gradient then results in potential energy dissipating as heat, instead of being converted to ATP, with rapid consumption of calories [27, 28]. The heat production represents a failure in thermoregulatory homeostasis, leading to uncontrolled hyperthermia [29].
Stimulation of Glycolysis
El-Guindy et al. concluded that dinitrophenol produces its glycolytic effect through its effect on the muscle contraction process [30]. Carbohydrate consumption markedly increases in the presence of dinitrophenol which allows for rapid weight loss when dinitrophenol is taken in small doses [26]. Pyruvic acid is aerobically metabolised to H2O and CO2, but results in the production of lactic acid when metabolised anaerobically. The discrepancy between the stimulation of glycolysis and the inhibition of oxidative phosphorylation results in a rapid rise in the production of pyruvic acid, leading to an increased production of lactic acid [24, 26, 31].
Potassium and Phosphate Accumulation
Mudge showed that potassium accumulates in rabbit kidney slices as the concentration of dinitrophenol is increased [32]. The accumulation of potassium continues even after cellular respiration is inhibited [32] and hyperkalaemia has contributed to toxicity [33]. Due to the uncoupling of oxidative phosphorylation, inorganic phosphate is no longer absorbed into the mitochondria and accumulation takes place, but whether this contributes to the clinical presentation is unknown [25, 34].
Teratogenicity, Carcinogenicity and Other Toxicity
In animal studies, DNP has been shown to be teratogenic, mutagenic and carcinogenic; developmental and reproductive toxicity has also been reported [35].
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Leef je uit.
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Ik zie genoeg serieuze reacties hoor. DNP afraden is gezien de toxiciteit verstandiger dan het gebruik faciliteren. Dat de meeste gekkies die het gebruiken, waaronder jij zelf, liever iets anders horen is een tweede.
Chill.NL
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Je hebt 2 liter bier en je hebt 2 liter Tequila.
Ano_09_01_24
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Net als met AAS doseringen verschillen de meningen over DNP hier ook per week zowat. Het ene moment pakt iedereen het en is het allemaal zo geweldig en het volgende moment moet je zweepslagen krijgen als je per ongeluk DNP schrijft.
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veroordeel dnp niet maar met deze hitte dnp pakken is niet bijster slim.
Ano_09_01_24
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Moet je je ogen opendoen.
