Properties of cardiac Ileak induced by photosensitizer-generated reactive oxygen

Tarr, Merrill; Arriaga, Edgar A.; Goertz, Kenneth K.; Valenzeno, Dennis Paul

doi:10.1016/0891-5849(94)90125-2

Cited by 24 publications

(27 citation statements)

References 18 publications

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“…In associated studies isolated membrane patches also showed an analogous permeability increase (44) , and this permeability pathway allowed passage of both sodium and calcium (45) . The latter is similar to results in whole cells showing that ILEAK is a relatively nonspecific cation pathway (26) . However, since the contracture seen in frog atrial cells is not identical to cell death, we assessed cell killing using cultured GH3 cells and 3 different assays of cell death.…”

Section: Ionic Currents and Cell Killingsupporting

confidence: 76%

“…For example, in freshly isolated cardiac cells the block of ionic currents, discussed above, precedes development of ILEAK, which is induced with complicated kinetics, when studied at a single voltage (22) . However, ILEAK is initially a K + current, but it becomes a mixed K + and Na + current as its magnitude increases (26) . A similar current in opposum kidney cells appears to be carried by both cations and anions (27) .…”

Section: Values Are Means ± Sem A) Exponential Rate Constants For mentioning

confidence: 99%

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Ion Currents as Initiators of Light-Induced Effects: Studies Using Photosensitizers

Valenzeno¹,

Tarr²

2000

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The effects of reactive oxygen species, especially as generated by photosensitizers and light, may serve as a model for light-induced effects relying on endogenous chromophores. Early events in the series of reactions initiated by these processes are reviewed and representative data on block of ionic currents, membrane permeabilization and increase in intracellular calcium concentration are presented. A general model for the effects of oxidative stress ranging from no effect with mild challenge to necrosis following severe challenge is presented. The results suggest that a 1 O2 mechanism could be operative for some forms of low level laser therapy. Energetic considerations suggest that this mechanism is only likely for irradiation wavelengths shorter than 1270 nm.

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Section: Ionic Currents and Cell Killingsupporting

confidence: 76%

Section: Values Are Means ± Sem A) Exponential Rate Constants For mentioning

confidence: 99%

Ion Currents as Initiators of Light-Induced Effects: Studies Using Photosensitizers

Valenzeno¹,

Tarr²

2000

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“…It inhibits an inward rectifier K+ current and activates a calcium-activated cationic current in rabbit ventricular cells (19). A similar photoactivated rose bengalinduced cationic current has been shown by Tarr et al (42) in frog cardiac cells. Moreover, Kuo et al (41) have suggested that the early cellular response to oxidative stress in nonexcitatory cells is the activation of K+ channels.…”

Section: Resultsmentioning

confidence: 62%

Susceptibility of cloned K+ channels to reactive oxygen species.

Duprat

Guillemare

Romey

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

178

112

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Free radical-induced oxidant stress has been implicated in a number of physiological and pathophysiological states including ischemia and reperfusion-induced dysrhythmia in the heart, apoptosis of T lymphocytes, phagocytosis, and neurodegeneration. We have studied the effects of oxidant stress on the native K+ channel from T lymphocytes and on K+ channels cloned from cardiac, brain, and Tlymphocyte cells and expressed in Xenopus oocytes. The activity of three Shaker K+ channels (Kvl.3, Kv1.4, and KvI.5), one Shaw channel (Kv3.4), and one inward rectifier K+ channel (IRK3) was drastically inhibited by photoactivation of rose bengal, a classical generator of reactive oxygen species. Other channel types (such as Shaker K+ channel Kv1.2, Shab channels Kv2.1 and Kv2.2, Shal channel Kv4.1, inward rectifiers IRKI and ROMK1, and hIsK) were completely resistant to this treatment. On the other hand tert-butyl hydroperoxide, another generator of reactive oxygen species, removed the fast inactivation processes of Kv1.4 and Kv3.4 but did not alter other channels. Xanthine/xanthine oxidase system had no effect on all channels studied. Thus, we show that different types of K+ channels are differently modified by reactive oxygen species, an observation that might be of importance in disease states.Molecular oxygen occupies an essential role in many of the metabolic processes associated with an aerobic existence. Oxidation and reduction reactions can lead to the formation of a variety of reactive oxygen species such as superoxide radicals (02), hydrogen peroxide (H202), hydroxyl radicals (OH-), or the long-lived diffusible singlet oxygen molecule (AgO2) (1, 2).These reactive oxygen species have been recently implicated in a variety of physiological and pathophysiological processes (3), such as apoptosis (for review, see ref. 4), cerebral ischemia (5), neurodegeneration (6), myocardial ischemia following reperfusion (7), or with heart failure in the hypertrophic heart (8).Voltage-sensitive K+ channels play an essential role in the generation of electrical activity in both neuronal and cardiac cells (9) but are also essential transport systems in a variety of other cell types such as T lymphocytes (10)

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“…The activation of the divalent cation-sensitive channel in embryonic epithelia is facilitated by acidosis (Sabovcik, Li, Kucera & Prod'Hom, 1995), suggesting a possible modulation by conditions such as ischaemia. It may be of interest to examine the influence of factors such as free reactive radicals or lysophospholipids, known to accumulate during ischaemia and to cause a modification in the activity of many channels and activation of other non-selective channels (Liu, Godhaber & Weiss, 1991;Tarr & Valenzeno, 1991;Tarr, Arriaga, Goertz & Valenzeno, 1994;Jabr & Cole, 1995;Magishi, Kimura, Kubo & Abiko, 1996). Our results may have implications for the mechanism underlying cell injury when Cafi is readmitted after a period of Cafi removal (the 'calcium paradox'; see Chapman & Tunstall, 1987) and for the basis of tissue preservation in Ca¥-free solutions (e.g.…”

Section: Discussionmentioning

confidence: 99%

Extracellular divalent cations block a cation non‐selective conductance unrelated to calcium channels in rat cardiac muscle

Mubagwa

Štengl

Flameng

1997

The Journal of Physiology

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The effect of removing extracellular divalent cations on resting potential (Vrest) and background conductance of rat cardiac muscle was studied. Vrest was measured with 3 M KCl‐filled microelectrodes in papillary muscles, or with a patch electrode in ventricular myocytes. Whole‐cell membrane currents were measured in myocytes using step or ramp voltage commands. In both muscles and single cells, decrease or removal of Ca2+o and Mg2+o caused a nifedipine‐resistant depolarization, which was reversed upon readmission of Ca2+o or Mg2+o (half‐maximal effect at 0.8 mM Ca2+o or 3 mM Mg2+o in muscles). In single myocytes, removal of Ca2+o and Mg2+o had no effect on the seal resistance in non‐ruptured cell‐attached recordings, but reversibly induced a current with a reversal potential (Vrev) of −8 ± 3.4 mV (with internal Cs+; mean. s.e.m., n= 23) during whole‐cell recordings. The current was insensitive to nifedipine (3–100 μM) or amiloride (1 mM). Vrev was insensitive to changes in the equilibrium potential for chloride ions (Ecl. The current induced in the absence of extracellular divalent cations was blocked in a concentration‐dependent manner by Ca2+o. (At −80 mV, the affinity constant Kca was 60 μM with a Hill coefficient of 0.9.) KCa was voltage dependent at positive but not negative potentials. Mg2+o, Ni2+o, Sr2+o, Ba2+o, Cd2+o and Gd3+o also blocked the current. In 0 mM Na+ (145 mM NMDG+), the inward component of the divalent cation‐sensitive current was decreased and Vrev shifted to more negative potentials. These results suggest that a novel conductance pathway, permeable to monovalent cations but not to OF and blocked by divalent cations, exists in ventricular myocytes.

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Properties of cardiac Ileak induced by photosensitizer-generated reactive oxygen

Cited by 24 publications

References 18 publications

Ion Currents as Initiators of Light-Induced Effects: Studies Using Photosensitizers

Ion Currents as Initiators of Light-Induced Effects: Studies Using Photosensitizers

Susceptibility of cloned K+ channels to reactive oxygen species.

Extracellular divalent cations block a cation non‐selective conductance unrelated to calcium channels in rat cardiac muscle

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