CO2 Exacerbates Oxygen Toxicity

[Lore]

Can someone translate this to Layman's language for me, please?

EMBO Rep. 2011 Apr;12(4):321-6. doi: 10.1038/embor.2011.7. Epub 2011 Feb 25.
CO2 exacerbates oxygen toxicity.
Ezraty B1, Chabalier M, Ducret A, Maisonneuve E, Dukan S.
Author information

Abstract
Reactive oxygen species (ROS) are harmful because they can oxidize biological macromolecules. We show here that atmospheric CO(2) (concentration range studied: 40-1,000 p.p.m.) increases death rates due to H(2)O(2) stress in Escherichia coli in a dose-specific manner. This effect is correlated with an increase in H(2)O(2)-induced mutagenesis and, as shown by 8-oxo-guanine determinations in cells, DNA base oxidation rates. Moreover, the survival of mutants that are sensitive to aerobic conditions (Hpx(-) dps and recA fur), presumably because of their inability to tolerate ROS, seems to depend on CO(2) concentration. Thus, CO(2) exacerbates ROS toxicity by increasing oxidative cellular lesions.

CO2 exacerbates oxygen toxicity. - PubMed - NCBI

 

[Lore]

and this one also, please

Consequences of hyperoxia and the toxicity of oxygen in the lung.
Mach WJ1, Thimmesch AR, Pierce JT, Pierce JD.
Author information

Abstract
Oxygen (O(2)) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O(2) species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair. Understanding the effects of O(2) administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.

Consequences of hyperoxia and the toxicity of oxygen in the lung. - PubMed - NCBI

 

[Hugh Johnson]

First seems to be about bacteria. The second is about pure oxygen.

 

[Lore]

First seems to be about bacteria. The second is about pure oxygen.

Thank you. I'm hypoxic on 3L oxygen 24/7, being diagnosed as emphysema C.O.P.D.. I believe there is an underlying cause for the hypoxia that I'm experiencing. I'm also unsure if I'm in a toxic condition and if so, how can I correct this condition. Many, many questions.

I'm also here to better understand oxygen, in layman's terms. I can understand medical journals and reports to a point, however, I need to speak with applicable individuals that will help me "comprehend & understand" and correct my understanding.

 

[InChristAlone]

Keep digging Peat has an entire lecture on this stuff on YouTube. CO2 is needed to use oxygen.

 

[Lore]

Thank God, it surely seems I've found a home ... I'm on the right track!!!

 

[Hugh Johnson]

Thank you. I'm hypoxic on 3L oxygen 24/7, being diagnosed as emphysema C.O.P.D.. I believe there is an underlying cause for the hypoxia that I'm experiencing. I'm also unsure if I'm in a toxic condition and if so, how can I correct this condition. Many, many questions.

I'm also here to better understand oxygen, in layman's terms. I can understand medical journals and reports to a point, however, I need to speak with applicable individuals that will help me "comprehend & understand" and correct my understanding.

Hard to say for certain,but you are probably lacking CO2, which means the oxygen can't get into the cells.

Hyperventilation, breathing excessively and causing too much carbon dioxide to be lost, is similar to being in the presence of too much oxygen; it’s similar to being at low altitude with high atmospheric pressure, only worse. Therefore, the physiological events produced by hyperventilation can give us an insight into what happens when the atmospheric pressure is low, by looking at the events in reverse. Likewise, breathing 100% oxygen has known harmful consequences, which are very similar to those produced by hyperventilation.
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Altitude and Mortality

 

[Owen B]

Hard to say for certain,but you are probably lacking CO2, which means the oxygen can't get into the cells.

Hyperventilation, breathing excessively and causing too much carbon dioxide to be lost, is similar to being in the presence of too much oxygen; it’s similar to being at low altitude with high atmospheric pressure, only worse. Therefore, the physiological events produced by hyperventilation can give us an insight into what happens when the atmospheric pressure is low, by looking at the events in reverse. Likewise, breathing 100% oxygen has known harmful consequences, which are very similar to those produced by hyperventilation.
​

Altitude and Mortality

Your quote about "breathing 100% oxygen" is just the issue I'm concerned about.

I have a friend in an assisted living facility and she's hooked up to one of those oxygen clips in her nose that you see all the time there and in hospitals. I know this is bad, but I don't know the science. I'll be looking at that Peat article.

 

[CLASH]

Hey Lore,
In regards to your emphysema and hypoxia I think the mechanism involves, having less surface area via the alveoli from which oxygen and CO2 can diffuse across. This is in conjunction with air becoming trapped in the lung. So from what I understand you have two situations occurring, 1) damage to the alveoli thus leading to difficult in diffusing the necessary gasses to and from the bloodstream and 2) gas from the bloodstream becoming trapped in the lung tissue at the lower levels. The causes of emphysema on a cellular level seems, at least to me, to be inflammation over the course of time within the lung, perhaps from smoking, air pollution, bacterial infection etc. This leads to the lung tissue first becoming inflamed, then becoming fibrosed and eventually possibly becoming calcified. The fibrosis and calcification occurs once the normal cells of the lung are damaged and subsequently killed leading the news cells (in the presence of the persistent inflammation) to develop as connective tissue as opposed to functional alveolar cells.

In regards to the CO2 and O2 concentrations in COPD patients, CO2 is elevated in the blood (hypercapnia) while O2 is lowered to an extent atleast from what I've read. Due to an inability of the lung tissue to properly expel CO2 from the bloodstream (the membrane which the CO2 crosses with the alveoli is damaged, as are the alveoli) CO2 builds up in the bloodstream. This build up is caused by the bodies metabolic processes such that cell metabolism produces CO2 and utilizes oxygen in the oxidation of energy substrates (i.e. sugar, fat). Interestingly, enough the medical establishment recommends a high fat low carb diet to avoid building up CO2 in the body because fat oxidation doesn't provide as much CO2 as sugar oxidation (the interest here is this is a main tenant of Peats philosophy i.e. CO2 is actually a good thing). As for the O2 in the blood it is lowered due to a decrease in diffusion across the alveolar membrane and constant utilization by the bodies cells.

The reason you are hypoxic on 3L is, I think, due to something called the Bohr effect. The effect is essentially this, when the surrounding tissue environment of a red blood cell has a high concentration of O2 the red blood cell unloads CO2 and loads O2. Then when the surrounding tissue of a red blood cell has a high concentration of CO2 the red blood cell unloads O2 and loads CO2. So if your cells are respiring at a high rate with sugar they are producing a high level of CO2. The high level of CO2 causes the red blood cell to unload its O2 to the cells to continue respiration while taking up the excess CO2 and transporting it to the lung. There at the lung a high level of O2 is present which causes the red blood cells to unload the CO2 and pick up the O2. With COPD the level of O2 at the lung is not as high due to the damage to the alveoli and the trapping of the air leading to higher CO2 levels and less unloading of CO2 by the red blood cells and thus less loading of O2. So what the doctors do is put the patient on O2 via nasal cannula to try and force the O2 levels higher in the lung so that the red blood cells can load the O2 and supply it to the tissues.

With all this in mind, the main mechanism for the issue is inflammation and damage to the alveolar membranes, at least from my perspective. If you could figure out what is eliciting this inflammation perhaps lung infection or actually a gut infection (asthma seems to be from what I've read a gut issue that leads the immune system to become hyperactive and respond to allergens in the lungs very strongly), smoking, or some type of toxin in your environment and eliminate it then you could start to possibly reverse the damage (In modern medicine this isn't viewed as possible so this is obviously my opinion).
Perhaps a stool test would help to determine if there is some type of inflammatory microbiota in the bowel and a ELISA/ACT LRA to determine delayed sensitivity, an allergy test, some blood test to look at hormones such as prolactin (to look at tissue serotonin and estrogen via Haidut/ Danny Roddy's provided info.), thyroid, basically all the peaty labs. To treat this in the meantime of uncovering the cause, perhaps PUFA depletion, aspirin, and Vit E all for the inflammation. Vit K for the fibrosis and calcification. Vit D for immune function with Vit A.

I'd just like to stipulate that all of this information is just my opinion, not medical advice. I am not a doctor. The information is based on what I've read, so please do your own research and talk to your doctor before trying anything.

Hope this helps