Duality of effect of La3+ on mitochondrial permeability transition pore depending on the concentration

被引：15

作者：

Dong, Shuai ^{[1
,2
]}

Zhao, Yuebin ^{[1
,2
]}

Liu, Huixue ^{[1
,2
]}

Yang, Xiaoda ^{[1
,2
]}

Wang, Kui ^{[1
,2
]}

机构：

[1] Peking Univ, Sch Pharmaceut Sci, Dept Biol Chem, Beijing 100083, Peoples R China

[2] Peking Univ, State Key Lab Nat & Biomimet Drug, Beijing 100083, Peoples R China

来源：

BIOMETALS | 2009年 / 22卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Lanthanum ion; Mitochondria; Calcium ion; Permeability transition pore; RAT-LIVER MITOCHONDRIA; CYCLOSPORINE-A; MEMBRANE-PERMEABILITY; CURCUMIN DERIVATIVES; BRAIN MITOCHONDRIA; INNER MEMBRANE; CYTOCHROME-C; CALCIUM; CA2+; MECHANISM;

D O I：

10.1007/s10534-009-9244-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In order to explore the role of mitochondria in proliferation promotion and/or apoptosis induction of lanthanum, the mutual influences between La3+ and Ca2+ on mitochondrial permeability transition pore (PTP) opening were investigated with isolated mitochondria from rat liver. The experimental results revealed that La3+ influence the state of mitochondria in a concentration-dependent biphasic manner. La3+ in nanomolar concentrations, acting as a Ca2+ analog, entered mitochondrial matrix via the RuR sensitive Ca2+ channel and elevated ROS level, leading to opening of PTP indicated by mitochondrial swelling, reduction of Delta I-m and cytochrome c release. Inhibition of PTP with 10 mu M CsA attenuated the effects of La3+. However, micromolar concentrations La3+ acted mainly as a Ca2+ antagonist, inhibiting PTP opening induced by Ca2+. We postulated that this action of La3+ on mitochondria through interaction with Ca2+ might be involved in the proliferation-promoting and apoptosis induction by La3+.

引用

页码：917 / 926

页数：10

共 31 条

[1]

ANNA C, 2004, FEBS LETT, V560, P63, DOI DOI 10.1016/S0014-5793(04)00071-7

[2] An examination of the secretion-like coupling model for the activation of the Ca2+ release-activated Ca2+ current ICRAC in RBL-1 cells [J].

Bakowski, D ;

Glitsch, MD ;

Parekh, AB .

JOURNAL OF PHYSIOLOGY-LONDON, 2001, 532 (01) :55-71

[3]

BEAVIS AD, 1985, J BIOL CHEM, V260, P3424

[4]

BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3

[5]

BROEKEMEIER KM, 1989, J BIOL CHEM, V264, P7826

[6] AMPA exposures induce mitochondrial Ca2+ overload and ROS generation in spinal motor neurons in vitro [J].

Carriedo, SG ;

Sensi, SL ;

Yin, HZ ;

Weiss, JH .

JOURNAL OF NEUROSCIENCE, 2000, 20 (01) :240-250

[7] RHODAMINE-123 AS A PROBE OF TRANSMEMBRANE POTENTIAL IN ISOLATED RAT-LIVER MITOCHONDRIA - SPECTRAL AND METABOLIC PROPERTIES [J].

EMAUS, RK ;

GRUNWALD, R ;

LEMASTERS, JJ .

BIOCHIMICA ET BIOPHYSICA ACTA, 1986, 850 (03) :436-448

[8] Calcium binding and translocation by the voltage-dependent anion channel: a possible regulatory mechanism in mitochondrial function [J].

Gincel, D ;

Zaid, H ;

Shoshan-Barmatz, V .

BIOCHEMICAL JOURNAL, 2001, 358 (358) :147-155

[9] Gadolinium inhibits thymidine incorporation and induces apoptosis in chondrocytes [J].

Greisberg, JK ;

Wolf, JM ;

Wyman, J ;

Zou, LJ ;

Terek, RM .

JOURNAL OF ORTHOPAEDIC RESEARCH, 2001, 19 (05) :797-801

[10] Mitochondrial permeability transition and oxidative stress [J].

Kowaltowski, AJ ;

Castilho, RF ;

Vercesi, AE .

FEBS LETTERS, 2001, 495 (1-2) :12-15

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