OXYGEN TOXICITY IN MAN

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author’s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual’s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.

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Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat

Journal of Applied Physiology ◽

10.1152/jappl.1980.48.3.505 ◽

1980 ◽

Vol 48 (3) ◽

pp. 505-510 ◽

Cited By ~ 1

Author(s):

L. Frank ◽

J. Summerville ◽

D. Massaro

Keyword(s):

Enzyme Activities ◽

Oxygen Toxicity ◽

Fetal Lung ◽

Antioxidant Enzyme Activities ◽

Newborn Rats ◽

Lung Maturation ◽

Lung Weight ◽

Pregnant Rats ◽

Rat Pups ◽

Hyperoxic Exposure

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.

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The genetics of catalase in Drosophila melanogaster: isolation and characterization of acatalasemic mutants.

Genetics ◽

10.1093/genetics/122.3.643 ◽

1989 ◽

Vol 122 (3) ◽

pp. 643-652 ◽

Cited By ~ 1

Author(s):

W J Mackay ◽

G C Bewley

Keyword(s):

Drosophila Melanogaster ◽

Free Radical ◽

Catalase Activity ◽

Oxygen Toxicity ◽

Threshold Effect ◽

Culture Conditions ◽

Free Radical Damage ◽

Isolation And Characterization ◽

Standard Culture ◽

Hypomorphic Alleles

Abstract Activated oxygen species have been demonstrated to be the important agents in oxygen toxicity by disrupting the structural and functional integrity of cells through lipid peroxidation events, DNA damage and protein inactivation. The biological consequences of free radical damage have long been hypothesized to be a causal agent in many aging-related diseases. Catalase (H2O2:H2O2 oxidoreductase; EC 1.15.1.1) is one of several enzymes involved in the scavenging of oxygen free radicals and free radical derivatives. The structural gene for catalase in Drosophila melanogaster has been localized to region 75D1-76A on chromosome 3L by dosage responses to segmental aneuploidy. This study reports the isolation of a stable deficiency, Df(3L)CatDH104(75C1-2;75F1), that uncovers the catalase locus and the subsequent isolation of six acatalasemic mutants. All catalase mutants are viable under standard culture conditions and recessive lethal mutations within the 75Cl-F1 interval have been shown not to affect catalase activity. Two catalase mutations are amorphic while four are hypomorphic alleles of the Cat+ locus. The lack of intergenic complementation between the six catalase mutations strongly suggests that there is only one functional gene in Drosophila. One acatalesemic mutation was mapped to position 3-47.0 which resides within the catalase dosage sensitive region. While complete loss of catalase activity confers a severe viability effect, residual levels are sufficient to restore viability to wild type levels. These results suggest a threshold effect for viability and offer an explanation for the general lack of phenotypic effects associated with the known mammalian acatalasemics.

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When anaerobes encounter oxygen: mechanisms of oxygen toxicity, tolerance and defence

Nature Reviews Microbiology ◽

10.1038/s41579-021-00583-y ◽

2021 ◽

Author(s):

Zheng Lu ◽

James A. Imlay

Keyword(s):

Oxygen Toxicity

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Modeling pulmonary and CNS O2 toxicity and estimation of parameters for humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00434.2001 ◽

2002 ◽

Vol 92 (1) ◽

pp. 248-256 ◽

Cited By ~ 23

Author(s):

R. Arieli ◽

A. Yalov ◽

A. Goldenshluger

Keyword(s):

Vital Capacity ◽

Oxygen Toxicity ◽

Recovery Process ◽

Likelihood Method ◽

Estimation Of Parameters ◽

Power Equation ◽

Hyperoxic Exposure ◽

Calculated Parameter ◽

Hyperbaric Oxygen Exposure ◽

Combined Data

10.1152/japplphysiol.00434.2001.—The power expression for cumulative oxygen toxicity and the exponential recovery were successfully applied to various features of oxygen toxicity. From the basic equation, we derived expressions for a protocol in which Po 2 changes with time. The parameters of the power equation were solved by using nonlinear regression for the reduction in vital capacity (ΔVC) in humans: %ΔVC = 0.0082 × t 2(Po 2/101.3)4.57, where t is the time in hours and Po 2is expressed in kPa. The recovery of lung volume is ΔVC t = ΔVCe × e −(−0.42 + 0.00379Po 2 ) t , where ΔVC t is the value at time tof the recovery, ΔVCe is the value at the end of the hyperoxic exposure, and Po 2 is the prerecovery oxygen pressure. Data from different experiments on central nervous system (CNS) oxygen toxicity in humans in the hyperbaric chamber ( n = 661) were analyzed along with data from actual closed-circuit oxygen diving ( n = 2,039) by using a maximum likelihood method. The parameters of the model were solved for the combined data, yielding the power equation for active diving: K = t 2(Po 2/101.3)6.8, where tis in minutes. It is suggested that the risk of CNS oxygen toxicity in diving can be derived from the calculated parameter of the normal distribution: Z = [ln( t) − 9.63 +3.38 × ln(Po 2/101.3)]/2.02. The recovery time constant for CNS oxygen toxicity was calculated from the value obtained for the rat, taking into account the effect of body mass, and yielded the recovery equation: Kt = K e × e −0.079 t , where Kt and K e are the values of K at time t of the recovery process and at the end of the hyperbaric oxygen exposure, respectively, and tis in minutes.

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EFFECTS OF 2-AMINO-2-HYDROXYMETHYL-1,3-PROPANEDIOL ON OXYGEN TOXICITY IN MICE*

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1961.tb45020.x ◽

1961 ◽

Vol 92 (2) ◽

pp. 710-723 ◽

Cited By ~ 12

Author(s):

Cyril Sanger ◽

Gabriel G. Nahas ◽

Allan R. Goldberg ◽

Gerard M. D'Alessio

Keyword(s):

Oxygen Toxicity

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