Interactions of Lanthanides with Tissues, Cells, and Cellular Organelles

Evans, Christopher H.

doi:10.1007/978-1-4684-8748-0_6

Cited by 7 publications

(2 citation statements)

References 280 publications

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“…However, details of the membrane phospholipid composition may alter the sensitivity to lanthanides. 34 It should be noted that lanthanides exert a number of other effects on membranes and their proteins. Consequently, the inhibition of the LPLCinduced current by lanthanides is not sufficient to establish that the LPLC-induced current results from an increase in membrane fluidity.…”

Section: Effects Of Lysolipids and Lanthanides On Membranesmentioning

confidence: 99%

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Plasmalogen-Derived Lysolipid Induces a Depolarizing Cation Current in Rabbit Ventricular Myocytes

Caldwell

Baumgarten

1998

Circulation Research

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Abstract-Plasmalogen rather than diacyl phospholipids are the preferred substrate for the cardiac phospholipase A 2 (PLA 2 ) isoform activated during ischemia. The diacyl metabolite, lysophosphatidylcholine, is arrhythmogenic, but the effects of the plasmalogen metabolite, lysoplasmenylcholine (LPLC), are essentially unknown. We found that 2.5 and 5 mol/L LPLC induced spontaneous contractions of intact isolated rabbit ventricular myocytes (median times, 27.4 and 16.4 minutes, respectively) significantly faster than lysophosphatidylcholine (Ͼ60 and 37.8 minutes, respectively). Whole-cell recordings revealed that LPLC depolarized the resting membrane potential from -83.5Ϯ0.2 to -21.5Ϯ1.0 mV. Depolarization was due to a guanidinium toxin-insensitive Na ϩ influx. The LPLC-induced current reversed at -18.5Ϯ0.9 mV and was shifted 26.7Ϯ4.2 mV negative by a 10-fold reduction of bath Na ϩ (Na ϩ /K ϩ permeability ratio, Ϸ 0.12Ϯ0.06). In contrast, block of Ca 2ϩ channels with Cd 2ϩ and reducing bath Cl -failed to affect the current. The actions of LPLC were opposed by lanthanides. Gd 3ϩ and La 3ϩ were equally effective inhibitors of the LPLC-induced current and equally delayed the onset of spontaneous contractions. However, the characteristics of lanthanide block imply that Gd 3ϩ -sensitive, poorly selective, stretch-activated channels were not involved. Instead, the data are consistent with the view that lanthanides increase phospholipid ordering and may thereby oppose membrane perturbations caused by LPLC. Plasmalogens constitute a significant fraction of cardiac sarcolemmal choline phospholipids. In light of their subclass-specific catabolism by phospholipase A 2 and the present results, it is suggested that LPLC accumulation may contribute to ventricular dysrhythmias during ischemia. (Circ Res. 1998;83:533-540.) Key Words: plasmalogen Ⅲ lysophosphatidylcholine Ⅲ ischemia Ⅲ lanthanide Ⅲ lysoplasmenylcholine A ltered membrane phospholipid metabolism is one of the earliest manifestations of myocardial ischemia. Phospholipase A 2 (PLA 2 ) is activated, 1-3 and lysophosphatidylcholine (LPC), a product of diacyl phospholipid catabolism, increases in tissue 4-6 and coronary effluents. [7][8][9] In addition to diacyl phospholipids, cardiac cell membranes contain plasmalogen phospholipids. Plasmalogens constitute 57% of choline phospholipids in canine sarcolemma 10 and Ͼ35% of total choline phospholipids in rabbit and human hearts.11 In contrast to the ester-linked fatty acid in diacyl phospholipids, the sn-1 position in plasmalogens contains an alkenyl ether moiety. Because of this structural feature, plasmalogens are metabolized differently from their diacyl counterparts. For instance, a Ca 2ϩ -independent PLA 2 rapidly activated during ischemia is reported to have a 16-fold higher reaction velocity with choline plasmalogen substrate than with phosphatidylcholine.2 This PLA 2 isoform also is present in human heart and is claimed to represent Ͼ95% of total PLA 2 activity.12 In addition, the rate of lysoplasmalogen removal from...

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Section: Effects Of Lysolipids and Lanthanides On Membranesmentioning

confidence: 99%

“…Published stability constants for gadolinium phosphate indicate that virtually no free Gd 3ϩ is available in phosphate-buffered media. 34,35 As a result, the ability of Gd 3ϩ to block the LPC-induced nonselective current in guinea pig myocytes remains an open question.…”

Section: Effects Of Lysolipids and Lanthanides On Membranesmentioning

confidence: 99%

Plasmalogen-Derived Lysolipid Induces a Depolarizing Cation Current in Rabbit Ventricular Myocytes

Caldwell

Baumgarten

1998

Circulation Research

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Interactions of Scandium and Yttrium within Cells, Cellular Organelles, and Tissues

Horovitz¹

2000

Biochemistry of Scandium and Yttrium, Part 2: Biochemistry and Applications

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Alterations in collagen metabolism and increased fibroproliferation in the heart in cerium-treated rats implications for the pathogenesis of endomyocardial fibrosis

Kumar

Shivakumar

1998

Biol Trace Elem Res

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Cerium (Ce), a rare earth element, has been postulated to play a role in the pathogenesis of tropical endomyocardial fibrosis (EMF). Investigations carried out recently in pursuance of the postulation furnished histological evidence of EMF and increased cardiac collagen content in rats on prolonged administration of Ce. The present study was undertaken to understand the molecular basis of myocardial injury and fibrosis produced by the element. This article presents evidence of increased lipid peroxidation and elevated rates of fibroblast proliferation and collagen deposition in the heart in Ce-treated rats. It is suggested that the element may trigger a wound-healing response in the cardiac tissue leading to cardiac fibrosis.

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Interactions of Lanthanides with Tissues, Cells, and Cellular Organelles

Cited by 7 publications

References 280 publications

Plasmalogen-Derived Lysolipid Induces a Depolarizing Cation Current in Rabbit Ventricular Myocytes

Plasmalogen-Derived Lysolipid Induces a Depolarizing Cation Current in Rabbit Ventricular Myocytes

Interactions of Scandium and Yttrium within Cells, Cellular Organelles, and Tissues

Alterations in collagen metabolism and increased fibroproliferation in the heart in cerium-treated rats implications for the pathogenesis of endomyocardial fibrosis

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