Diving seals: are they a model for coping with oxidative stress?

Zenteno‐Savín, Tania; Clayton-Hernández, E; Elsner, Robert

doi:10.1016/s1532-0456(02)00075-3

Cited by 51 publications

(48 citation statements)

References 48 publications

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“…This globin, discovered about a decade ago (Burmester et al, 2000), is thought to play a key role for maintenance of aerobic metabolism in neural tissue, possibly by facilitating O 2 diffusion ). However, neuroglobin may also have other functions related to hypoxia defense, such as the detoxification of reactive oxygen species (ROS) ) that are generated during and after diving (Zenteno-Savín et al, 2002). Interestingly, studies in the deep-diving hooded seal (Cystophora cristata) have revealed that their cerebral neuroglobin levels are not higher than those of rodents or man (Mitz et al, 2009).…”

Section: O 2 Diffusion and Possible Roles Of Neuroglobinmentioning

confidence: 99%

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

Larson

Drew

Folkow

et al. 2014

Journal of Experimental Biology

126

101

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Many vertebrates are challenged by either chronic or acute episodes of low oxygen availability in their natural environments. Brain function is especially vulnerable to the effects of hypoxia and can be irreversibly impaired by even brief periods of low oxygen supply. This review describes recent research on physiological mechanisms that have evolved in certain vertebrate species to cope with brain hypoxia. Four model systems are considered: freshwater turtles that can survive for months trapped in frozen-over lakes, arctic ground squirrels that respire at extremely low rates during winter hibernation, seals and whales that undertake breath-hold dives lasting minutes to hours, and naked mole-rats that live in crowded burrows completely underground for their entire lives. These species exhibit remarkable specializations of brain physiology that adapt them for acute or chronic episodes of hypoxia. These specializations may be reactive in nature, involving modifications to the catastrophic sequelae of oxygen deprivation that occur in non-tolerant species, or preparatory in nature, preventing the activation of those sequelae altogether. Better understanding of the mechanisms used by these hypoxiatolerant vertebrates will increase appreciation of how nervous systems are adapted for life in specific ecological niches as well as inform advances in therapy for neurological conditions such as stroke and epilepsy.KEY WORDS: Arctic ground squirrel, Cetacean, Hypoxia, Naked mole-rat, Seal, Turtle IntroductionEnvironmental conditions vary enormously for vertebrates, both with respect to the extreme conditions tolerated by a given species at different times and with respect to average living conditions tolerated by different species. Temperature is perhaps the most obvious example: from the poles to the equator, average ambient temperatures vary widely and have been accompanied by physiological adaptations appropriate to resident species; seasonal variations in temperature and resource variability can induce dramatic changes in physiological and/or behavioral patterns including migration and hibernation. Oxygen levels also vary widely, with animals adapted to sea level, high-altitude, underground and aquatic habitats. Oxygen levels can also change dramatically on a shorter-term basis, as can occur in tidal pools or in breath-hold divers. Approximately 20% of the oxygen consumed by the human body is used by the brain. The greater part of this oxygen is used to produce the ATP required to maintain the membrane potentials necessary for electrical signaling with synaptic and action potentials (Harris et al., 2012). In many vertebrates, including adult humans, interruption of the oxygen supply to the brain for more than a few minutes leads to irreversible neurological damage, including neuronal death. Without oxidative phosphorylation, ATP-dependent neuronal processes including ion transport and neurotransmitter reuptake decline sharply. Without pumping, ion gradients fail and neurons depolarize, releasing excessive levels...

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Section: O 2 Diffusion and Possible Roles Of Neuroglobinmentioning

confidence: 99%

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

Larson

Drew

Folkow

et al. 2014

Journal of Experimental Biology

126

101

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“…The role of HIF-1 as a physiological mediator of the protective effects of ischemic preconditioning has been extensively demonstrated (Bergeron et al, 2000;Grimm et al, 2005;Semenza, 2000b). The observed increases in HIF-1 nuclear content after repetitive breath-holds suggest that rest-and voluntary submersion-associated apneas also contribute to the preconditioning of the seal's muscle by activating the HIF-1-mediated adaptive response to hypoxia (Johnson et al, 2004;Johnson et al, 2005;Zenteno-Savín et al, 2002). The observed increase in Mb further supports the latter idea as Mb is upregulated in response to hypoxia in mammalian tissues and cells (Kanatous and Mammen, 2010), and without physical activity in vertebrates adapted to dive such as penguins and seals (Noren et al, 2005).…”

Section: Eupneamentioning

confidence: 99%

“…Apnea in seals is characterized by a series cardiovascular adjustments (reduction in cardiac output, bradycardia, peripheral vasoconstriction) that allow seals to maximize the use of their oxygen stores but at the same time result in blood oxygen depletion and blood flow redistribution towards obligatory oxygendependent tissues, exposing seals to critical levels of ischemia and hypoxemia (Castellini et al, 1994;Elsner, 1999;Kooyman and Ponganis, 1998;Stockard et al, 2007). At the end of an apnea bout, an increase in cardiac output and ventilation restores blood flow to tissues and blood oxygen content, presenting seals with potential increases in oxidant production and oxidative stress (Elsner et al, 1998;Zenteno-Savín et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…An enhanced antioxidant capacity likely contributes to the seal's tolerance to apnea-induced hypoxemia and ischemia/reperfusion (Hermes-Lima and Zenteno-Savín, 2002;Zenteno-Savín et al, 2002). Plasma, tissues and RBCs of seals possess higher basal activities of several antioxidant enzymes and higher glutathione (GSH) levels than those of terrestrial mammals (Murphy and Hochachka, 1981 .…”

Section: Introductionmentioning

confidence: 99%

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Apnea stimulates the adaptive response to oxidative stress in elephant seal pups

Vázquez‐Medina

Zenteno‐Savín

Tift

et al. 2011

Journal of Experimental Biology

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SUMMARYExtended breath-hold (apnea) bouts are routine during diving and sleeping in seals. These apneas result in oxygen store depletion and blood flow redistribution towards obligatory oxygen-dependent tissues, exposing seals to critical levels of ischemia and hypoxemia. The subsequent reperfusion/reoxygenation has the potential to increase oxidant production and thus oxidative stress. The contributions of extended apnea to oxidative stress in adapted mammals are not well defined. To address the hypothesis that apnea in seals is not associated with increased oxidative damage, blood samples were collected from northern elephant seal pups (N6) during eupnea, rest-and voluntary submersion-associated apneas, and post-apnea (recovery). Plasma 4-hydroxynonenal (HNE), 8-isoprostanes (8-isoPGF 2 ), nitrotyrosine (NT), protein carbonyls, xanthine and hypoxanthine (HX) levels, along with xanthine oxidase (XO) activity, were measured. Protein content of XO, superoxide dismutase 1 (Cu,ZnSOD), catalase and myoglobin (Mb), as well as the nuclear content of hypoxia inducible factor 1 (HIF-1) and NF-E2-related factor 2 (Nrf2), were measured in muscle biopsies collected before and after the breath-hold trials. HNE, 8-iso PGF 2 , NT and protein carbonyl levels did not change among eupnea, apnea or recovery. XO activity and HX and xanthine concentrations were increased at the end of the apneas and during recovery. Muscle protein content of XO, CuZnSOD, catalase, Mb, HIF-1 and Nrf2 increased 25-70% after apnea. Results suggest that rather than inducing the damaging effects of hypoxemia and ischemia/reperfusion that have been reported in non-diving mammals, apnea in seals stimulates the oxidative stress and hypoxic hormetic responses, allowing these mammals to cope with the potentially detrimental effects associated with this condition.

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“…This globin, discovered about a decade ago (Burmester et al, 2000), is thought to play a key role for maintenance of aerobic metabolism in neural tissue, possibly by facilitating O 2 diffusion (Burmester and Hankeln, 2009). However, neuroglobin may also have other functions related to hypoxia defense, such as the detoxification of reactive oxygen species (ROS) (Burmester and Hankeln, 2009) that are generated during and after diving (Zenteno-Savín et al, 2002). Interestingly, studies in the deep-diving hooded seal (Cystophora cristata) have revealed that their cerebral neuroglobin levels are not higher than those of rodents or man (Mitz et al, 2009).…”

Section: O 2 Diffusion and Possible Roles Of Neuroglobinmentioning

confidence: 99%

Cellular Basis for Learning Impairment in Fragile X Syndrome

Larson¹

2014

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information , 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE August 2014 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Illinois at Chicago PERFORMING ORGANIZATION REPORT NUMBERChicago, IL 60612-4305 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThis research combines behavioral, electrophysiological, and molecular approaches to elucidate the cellular basis for learning impairment in Fragile X Syndrome (FXS), using olfactory learning in Fmr1-KO mice as a model system. We hypothesize that FMRP, the protein missing in FXS, participates in two aspects of circuit function that are critical to learning: synaptic plasticity and the generation and survival of new neurons in the adult brain. Efforts in the second year of support were directed toward establishing a method to specifically upregulate neurogenesis in adult fragile X mice, test fragile X mice for learning deficits in hippocampal-independent tasks, and determine if learning affects NMDA receptor trafficking to synapses. Significant advances have been made in the establishment of behavioral paradigms to test both hippocampal -dependent and -independent forms of olfactory learning. Experimental paradigms have also been refined for the study of neurogenesis in the olfactory bulb, glutamate receptor expression as it relates to olfactory learning in olfactory cortex and hippocampus, and the effects of aging on glutamate receptor expression. These studies are likely to advance our understanding of intellectual disability and autism in addition to the specific condition of fragile X syndrome. This knowledge will be necessary for the development of rational strategies for prevention and treatment of cognitive impairments from a variety of causes. SUBJECT TERMSFragile X Syndrome, synaptic plasticity, long-term potentiation, glutamate receptors, neurogenesis, olfactory learning INTRODUCTIONFragile X syndrome is the most common inherited form of intellect...

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Diving seals: are they a model for coping with oxidative stress?

Cited by 51 publications

References 48 publications

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

No oxygen? No problem! Intrinsic brain tolerance to hypoxia in vertebrates

Apnea stimulates the adaptive response to oxidative stress in elephant seal pups

Cellular Basis for Learning Impairment in Fragile X Syndrome

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