Does Oxygen REALLY not contribute to DCS

[rjack321]

What is the rate limiting step in metabolism of oxygen? I vaguely remember something about mitochondria and stuff, but I am a geochemist (err, lawyer) not a biologist.

Typically O2 is the limiting piece of the krebs cycle. That's why you make lactic acid and sprinting muscles get tired easily.

So with an excess of O2, I'd guess that maybe the release of P from ATP might be a limiting step??

Lynne your turn...

 

[pescador775]

dwalke, you got your answer from TSM. Oxygen irritates the lungs and the "clock" is calculated to prevent pneumonia. Oxygen toxicity to the CNS is primarily PP related, acts on the CNS in unknown ways (unknown to me), and is different in physiology from what I understand is the raison d'etre of the clock.

 

[pescador775]

Typically O2 is the limiting piece of the krebs cycle. That's why you make lactic acid and sprinting muscles get tired easily.

So with an excess of O2, I'd guess that maybe the release of P from ATP might be a limiting step??

Lynne your turn...

That sounds like nonsense. I don't know what the answer is but it's not that. I'll take a wild guess although I don't really care about the mechanism as much as prevention. My WAG, oxygen interferes with cholinesterase in some way.

 

[pescador775]

Use your imagination on this one, oxygen is not all bad.

Oct. 25, 2005 — Supplemental oxygen can reduce surgical site infections (SSI), according to the results of a double-blind, randomized trial published in the Oct. 26 issue of JAMA. The editorialists suggest that surgeons should encourage use of higher oxygen tensions.

"Supplemental perioperative oxygen has been variously reported to halve or double the risk of surgical wound infection," write F. Javier Belda, MD, PhD, from the Hospital Clínico Universitario in Valencia, Spain, and colleagues from the Spanish Reduccion de la Tasa de Infeccion Quirurgica Group. "Infection risk depends on tissue oxygen partial pressure and, therefore, interventions that increase tissue oxygen may reduce infection risk."

 

[dsteding]

That sounds like nonsense. I don't know what the answer is but it's not that. I'll take a wild guess although I don't really care about the mechanism as much as prevention. My WAG, oxygen interferes with cholinesterase in some way.

Pescador-

Your reference to cholinesterase is presumably relating to the biochemical mechanism of O2 toxicity. I think rjack's response is to my question.

To clarify, we weren't talking about the biochemical basis for O2 toxcity but whether you can, despite your body metabolizing oxygen, overwhelm the rate of that metabolism and saturate your tissues with O2. If you can, it should off-gas in a similar manner to an inert gas, but to answer that question one would have to look at the maximum rate of metabolism versus rate of ongassing . . . and all this is would have to happen at PPO2s of below, say 1.6 to 2.0, at which O2 tox becomes the physiological response.

 

[dlwalke]

OTUs are limited to let the cellular damage caused by the O2 heal. The O2 itself is long gone.

Its very hard to get close to the OTU limits unless you're diving 5-10 times a day on high ppO2 for several days in a row.

OK. Anyone know what kind of damage that is? Is oxygen or a product of the oxygen in Nitrox acting as a free radical? Is it that kind of damage? I imagine if it were a real problem, it would be well known and previously discussed, but that doesn't sound good. To quote a snippet from Time magazine I just found on the web

"Free radicals are cellular renegades; they wreak havoc by damaging DNA, altering biochemical compounds, corroding cell membranes and killing cells outright. Such molecular mayhem, scientists increasingly believe, plays a major role in the development of ailments like cancer, heart or lung disease and cataracts. Many researchers are convinced that the cumulative effects of free radicals also underlie the gradual deterioration that is the hallmark of aging in all individuals, healthy as well as sick.

Not to be an alarmist or anything. Maybe its a different kind of reaction. If not, maybe I'll switch to EANx10.

 

[dsteding]

My guess is that the high PPO2 results in oxygen generating free radicals in tissue that in turn cause cellular damage. Seems to me I remember that free radicals are regularly generated in cells from 02 but there are enough biochemical buffers to keep those free radicals at acceptable levels.

My toxicology professor's voice is rattling around in my head, I think epoxides are somehow involved in the whole entire free radical generation process . . . but that class was long ago.

 

[lamont]

OK, I think I understand...maybe. Is it the case then that oxygen toxicity is not due to the buildup of O2 bubbles, but instead of non-gaseous oxygen. In other words, is the purpose of the "oxygen clock" NOT to let O2 bubbles offgas, but to let the levels of oxygen in some other form approach basal values or, alternatively, to let the physiological consequences of previous oxygen exposure dissipate?

The "alternatively, to let the physiological consequences of previous oxygen exposure dissipate" bit is more correct. The clock has nothing to do with O2 being leftover anywhere, its the effects of O2 exposure that are leftover.

 

[lamont]

At high partial pressures, is it possible to overload tissues, namely overwhelm a cell's ability to metabolize oxygen, causing super-saturation?

To get O2 bends you need to saturate O2 binding to hemoglobin in order to produce free O2 which can then dissolve into tissues. That happens only at levels above 1.6 ppO2 so it isn't relevant to diving.

 

[do it easy]

Back on topic, I believe, the OP was asking about DCS. I believe Haldane did some experiments with goats breathing pure oxygen under pressure and then released the pressure to simulate an ascent. They exhibited DCS like symptoms which cleared relatively quickly. I think this was effectively oxygen DCS, so it might be possible in humans.