Cadmium affects metabolic responses to prolonged anoxia and reoxygenation in eastern oysters (Crassostrea virginica)

2009 ◽  
Vol 297 (5) ◽  
pp. R1262-R1272 ◽  
Author(s):  
I. O. Kurochkin ◽  
A. V. Ivanina ◽  
S. Eilers ◽  
C. A. Downs ◽  
L. A. May ◽  
...  
Keyword(s):  
Crassostrea Virginica ◽  
Oxygen Deficiency ◽  
Respiratory Control ◽  
Maximum Activity ◽  
Dna Lesions ◽  
Metabolic Responses ◽  
Coastal Zones ◽  
Mitochondrial Uncoupling ◽  
Eastern Oysters ◽  
Stimulation Of

Benthic marine organisms such as mollusks are often exposed to periodic oxygen deficiency (due to the tidal exposure and/or seasonal expansion of the oxygen-deficient dead zones) and pollution by metals [e.g., cadmium, (Cd)]. These stressors can strongly affect mollusks' survival; however, physiological mechanisms of their combined effects are not fully understood. We studied the effects of Cd exposure on metabolic responses to prolonged anoxia and subsequent recovery in anoxia-tolerant intertidal mollusks Crassostrea virginica (eastern oysters). Anoxia led to an onset of anaerobiosis indicated by accumulation of l-alanine, acetate, and succinate. Prolonged anoxia (for 6 days) caused a decline in the maximum activity of electron transport chain and ADP-stimulated ( state 3) oxygen uptake by mitochondria (MO2), but no change in the resting ( state 4) MO2 of oyster mitochondria, along with a slight but significant reduction of mitochondrial respiratory control ratio. During reoxygenation, there was a significant overshoot of mitochondrial MO2 (by up to 70% above the normoxic steady-state values) in control oysters. Mild mitochondrial uncoupling during prolonged shutdown in anoxic tissues and a subsequent strong stimulation of mitochondrial flux during recovery may help to rapidly restore redox status and protect against elevated reactive oxygen species formation in oysters. Exposure to Cd inhibits anaerobic metabolism, abolishes reoxygenation-induced stimulation of mitochondrial MO2, and leads to oxidative stress (indicated by accumulation of DNA lesions) and a loss of mitochondrial capacity during postanoxic recovery. This may result in increased sensitivity to intermittent hypoxia and anoxia in Cd-exposed mollusks and will have implications for their survival in polluted estuaries and coastal zones.

Interactive effects of cadmium and hypoxia on metabolic responses and bacterial loads of eastern oysters Crassostrea virginica Gmelin

Chemosphere ◽  
2011 ◽  
Vol 82 (3) ◽  
pp. 377-389 ◽  
Author(s):  
Anna V. Ivanina ◽  
Brett Froelich ◽  
Tiffany Williams ◽  
Eugene P. Sokolov ◽  
James D. Oliver ◽  
...  
Keyword(s):  
Crassostrea Virginica ◽  
Interactive Effects ◽  
Metabolic Responses ◽  
Eastern Oysters

scholarly journals Oyster hatchery breakthrough of two HABs and potential effects on larval eastern oysters (Crassostrea virginica)

Harmful Algae ◽  
2021 ◽  
Vol 101 ◽  
pp. 101965
Author(s):  
Sarah K.D. Pease ◽  
Kimberly S. Reece ◽  
Jeffrey O'Brien ◽  
Patrice L.M. Hobbs ◽  
Juliette L. Smith
Keyword(s):  
Crassostrea Virginica ◽  
Eastern Oysters

scholarly journals Metabolic effect of α-and the β-adrenergic stimulation of rat submaxillary gland in vitro

1976 ◽  
Vol 160 (3) ◽  
pp. 597-601 ◽  
Author(s):  
M P Thompson ◽  
D H Williamson
Keyword(s):  
Submaxillary Gland ◽  
Metabolic Effect ◽  
Metabolic Responses ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Presence And Absence ◽  
Stimulation Of

1. Incubation of submaxillary-gland slices with isoproterenol, a β-adrenergic agonist, stimulated glucose removal by 41% and decreased tissue [glucose 6-phosphate] by 50%. Propranolol blocked these effects of isoproterenol. 2. Phenylephrine, an α-adrenergic agonist, stimulated glucose removal by 35% and decreased tissue [glucose 6-phosphate] by 75%. In addition, phenylephrine also completely overcame the inhibition of pyruvate removal caused by acetoacetate metabolism and decreased tissue [atp] by 45%. Phentolamine blocked the effects of phenylephrine. 3. In contrast with β-adrenergic stimulation, α-adrenergic stimulation required exogenous Ca2+. 4. These results explain the different metabolic responses of the submaxillary gland to adrenaline in the presence and absence of exogenous Ca2+.

Parabrachial units responding to stimulation of buffer nerves and forebrain in the cat

1983 ◽  
Vol 245 (6) ◽  
pp. R811-R819 ◽  
Author(s):  
D. F. Cechetto ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Respiratory Control ◽  
Firing Frequency ◽  
Central Nucleus ◽  
Paraventricular Nuclei ◽  
Control Signals ◽  
Parabrachial Nuclei ◽  
Excitatory Responses ◽  
Stimulation Of

Spontaneously firing units in the region of parabrachial nuclei (PB) and Kolliker-Fuse nuclei (KF) of 19 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves, of central nucleus of the amygdala (ACE), and of paraventricular nuclei of the hypothalamus (PVH). In the ipsilateral PB 64 of 189 and in the contralateral PB 9 of 103 units responded to CSN stimulation; 18 of 185 ipsilaterally and 7 of 97 contralaterally responded to ADN stimulation. Responses were primarily excitatory, and units were located primarily in the ventrolateral portion of the PB. Only 9 of 267 units responded to stimulation of both CSN and ADN. Stimulation of the ACE and PVH antidromically activated 9 and 7 units, respectively, in PB and approximately half of these also responded to buffer nerve stimulation. In the ipsilateral PB 56 of 207 and in the contralateral PB 11 of 103 units responded orthodromically to ACE stimulation, and 23 of 177 ipsilaterally and 2 of 103 contralaterally responded orthodromically to PVH stimulation with primarily excitatory responses and were located primarily in the ventrolateral portion of the PB and KF. Of these units approximately half also responded to buffer nerve stimulation. These results suggest an important role for PB-KF in mediating ascending and descending cardiovascular and respiratory control signals.

A Respiratory Reflex as Affected by an Anticholinesterase

1956 ◽  
Vol 185 (1) ◽  
pp. 142-144 ◽  
Author(s):  
Bernard Metz
Keyword(s):  
Electrical Stimulation ◽  
Respiratory Failure ◽  
Respiratory Control ◽  
Reflex Response ◽  
Suggestive Evidence ◽  
Small Doses ◽  
Respiratory Reflex ◽  
Stimulation Of

Small doses of the potent anticholinesterase, TEPP, introduced via a cisternal puncture produce a marked potentiation of the respiratory reflex response induced by electrical stimulation of Hering's nerve in the dog. Larger doses of TEPP cause an inhibition of this reflex followed by respiratory failure. These experiments lend suggestive evidence that a neurohumoral mediator (e.g. acetylcholine) may be a component of respiratory control.

Biological Assessment of Eastern Oysters (Crassostrea virginica) Inhabiting Reef, Mangrove, Seawall, and Restoration Substrates

2013 ◽  
Vol 37 (4) ◽  
pp. 962-972 ◽  
Author(s):  
Michael Drexler ◽  
Melanie L. Parker ◽  
Stephen P. Geiger ◽  
William S. Arnold ◽  
Pamela Hallock
Keyword(s):  
Crassostrea Virginica ◽  
Biological Assessment ◽  
Eastern Oysters

Rapid and transient excitation of respiration mediated by central chemoreceptor

1988 ◽  
Vol 64 (4) ◽  
pp. 1369-1375 ◽  
Author(s):  
H. Arita ◽  
N. Kogo ◽  
K. Ichikawa
Keyword(s):  
Control System ◽  
Dynamic Properties ◽  
Respiratory Rhythm ◽  
Respiratory Control ◽  
Facilitatory Effect ◽  
Onset Latency ◽  
Central Chemoreceptors ◽  
Spontaneously Breathing ◽  
Respiratory Phases ◽  
Stimulation Of

We evaluated rapid and transient changes in phrenic nerve (PN) and internal intercostal (IIC) activities when 0.2-0.5 ml of saline saturated with 100% CO2 was injected into the vertebral artery during various respiratory phases in decerebrated spontaneously breathing cats. The injections evoked an initial transient inhibition of ongoing PN or IIC activity with a mean onset latency of 0.17 s, followed by excitation of subsequent respiratory activities with an onset latency ranging from 0.4 to 2.7 s; the average onset latency of expiratory excitation (1.49 s) was significantly longer than that of inspiratory facilitation (0.89 s). The initial inhibitory responses were analogous to reflex effects of injections of phenyl biguanide, indicating that the initial inhibition was due to activation of vascular nociceptors and the subsequent excitation was due to stimulation of the central chemoreceptors. In addition, CO2-saline injections during hypocapnic apnea developed a quick reappearance of respiratory rhythm, and the first facilitatory effect appeared in tonic IIC activity, which became more active before rhythm started. In summary, the present study, by use of a technique of vertebral arterial injections of 100% CO2-saline, revealed dynamic properties of respiratory control system mediated by central chemoreceptors and vascular nociceptors.

Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats

1980 ◽  
Vol 49 (5) ◽  
pp. 769-777 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora
Keyword(s):  
Control Systems ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Monoamine Metabolism ◽  
Moderate Hypoxia ◽  
Significant Depression ◽  
Brain Monoamine ◽  
Conscious Animals ◽  
Ventilatory Response To Hypoxia ◽  
Stimulation Of

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.

Sign in / Sign up

Export Citation Format

Share Document