meatbag
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Originally posted by the scholar @md_a here: Corona Virus How To Treat
"Regarding the article
Ray Peat:
"The article sounds to me like the ideas of students who have taken a pharmacology course in computer modeling of molecules; without an anchor to experiment, it’s perfectly useless. Iron and particulate pollution cause lung damage similar to the inflammation produced by the virus. Ventilating patients decreases their antiinflammatory CO2, making the inflammation worse. Acetaminophen, often given to patients, increases lung nitric oxide and damages red blood cells, adding to the harm done by treatment. The suggested treatments could aggravate the damage; for example, chloroquine increases nitric oxide. The angiotensin produced in response to the virus increases nitric oxide, and blocking that protects from the virus."
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J Clin Invest. 1998 Aug 1; 102(3): 595–605.
Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.
D Ghigo, E Aldieri, R Todde, C Costamagna, G Garbarino, G Pescarmona, and A Bosia
Abstract
Nitric oxide (NO) is a free radical involved in the regulation of many cell functions and in the expression of several diseases. We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms. Increased NO synthesis is, at least partly, responsible for chloroquine-induced inhibition of cell proliferation: indeed, NOS inhibitors revert the drug-evoked blockage of mitogenesis and ornithine decarboxylase activity in murine and porcine endothelial cells. The NOS-activating effect of chloroquine is dependent on its weak base properties, as it is exerted also by ammonium chloride, another lysosomotropic agent. Both compounds activate NOS by limiting the availability of iron: their stimulating effects on NO synthesis and inhibiting action on cell proliferation are reverted by iron supplementation with ferric nitrilotriacetate, and are mimicked by incubation with desferrioxamine. Our results suggest that NO synthesis can be stimulated in endothelial cells by chloroquine via an impairment of iron metabolism.
"Regarding the article
Ray Peat:
"The article sounds to me like the ideas of students who have taken a pharmacology course in computer modeling of molecules; without an anchor to experiment, it’s perfectly useless. Iron and particulate pollution cause lung damage similar to the inflammation produced by the virus. Ventilating patients decreases their antiinflammatory CO2, making the inflammation worse. Acetaminophen, often given to patients, increases lung nitric oxide and damages red blood cells, adding to the harm done by treatment. The suggested treatments could aggravate the damage; for example, chloroquine increases nitric oxide. The angiotensin produced in response to the virus increases nitric oxide, and blocking that protects from the virus."
---
J Clin Invest. 1998 Aug 1; 102(3): 595–605.
Chloroquine stimulates nitric oxide synthesis in murine, porcine, and human endothelial cells.
D Ghigo, E Aldieri, R Todde, C Costamagna, G Garbarino, G Pescarmona, and A Bosia
Abstract
Nitric oxide (NO) is a free radical involved in the regulation of many cell functions and in the expression of several diseases. We have found that the antimalarial and antiinflammatory drug, chloroquine, is able to stimulate NO synthase (NOS) activity in murine, porcine, and human endothelial cells in vitro: the increase of enzyme activity is dependent on a de novo synthesis of some regulatory protein, as it is inhibited by cycloheximide but is not accompanied by an increased expression of inducible or constitutive NOS isoforms. Increased NO synthesis is, at least partly, responsible for chloroquine-induced inhibition of cell proliferation: indeed, NOS inhibitors revert the drug-evoked blockage of mitogenesis and ornithine decarboxylase activity in murine and porcine endothelial cells. The NOS-activating effect of chloroquine is dependent on its weak base properties, as it is exerted also by ammonium chloride, another lysosomotropic agent. Both compounds activate NOS by limiting the availability of iron: their stimulating effects on NO synthesis and inhibiting action on cell proliferation are reverted by iron supplementation with ferric nitrilotriacetate, and are mimicked by incubation with desferrioxamine. Our results suggest that NO synthesis can be stimulated in endothelial cells by chloroquine via an impairment of iron metabolism.