DNA strand scission and PC12 cell death induced by salsolinol and copper

Hyun Jung Kim; Hye Ran Yoon; Stacy Washington; In I. Chang; Young J. Oh; Young Joon Surh

doi:10.1016/S0304-3940(97)00866-5

DNA strand scission and PC12 cell death induced by salsolinol and copper

Hyun Jung Kim, Hye Ran Yoon, Stacy Washington, In I. Chang, Young J. Oh, Young Joon Surh

Department of Systems Biology

Research output: Contribution to journal › Article › peer-review

24 Citations (Scopus)

Abstract

The naturally occurring neurotoxin, 1-methyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline (salsolinol; SAL), has been speculated to contribute to Parkinson's disease and neuropathology of chronic alcoholism. In the present study, we found the capability of SAL to cause DNA cleavage in the presence of Cu(II). Incubation of SAL and CuCl₂ with calf thymus DNA caused strand breaks. Likewise, SAL in combination with Cu(II) mediated the strand scission in φX174 RFI supercoiled DNA in a time-related manner. Neither Cu(II) nor the catechol alone induced any appreciable DNA cleavage. The reaction of SAL with Cu(II) was accompanied by the reduction of Cu(II) to Cu(I). Furthermore, SAL induced cell death in cultured PC12 cells which was exacerbated by Cu(II). From these data, it seems likely that SAL undergoes redox cycling catalyzed by Cu(II) to generate reactive species which may be responsible for the neurotoxic action of this catechol isoquinoline.

Original language	English
Pages (from-to)	95-98
Number of pages	4
Journal	Neuroscience Letters
Volume	238
Issue number	3
DOIs	https://doi.org/10.1016/S0304-3940(97)00866-5
Publication status	Published - 1997 Dec 5

Bibliographical note

Funding Information:
This work was supported by the '96 Genetic Engineering Research Grant (to Y.-J.S.) from the Ministry of Education and in part by STEPI B-02-08-04 (to Y.J.O.), Republic of Korea.

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10.1016/S0304-3940(97)00866-5

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title = "DNA strand scission and PC12 cell death induced by salsolinol and copper",

abstract = "The naturally occurring neurotoxin, 1-methyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline (salsolinol; SAL), has been speculated to contribute to Parkinson's disease and neuropathology of chronic alcoholism. In the present study, we found the capability of SAL to cause DNA cleavage in the presence of Cu(II). Incubation of SAL and CuCl2 with calf thymus DNA caused strand breaks. Likewise, SAL in combination with Cu(II) mediated the strand scission in φX174 RFI supercoiled DNA in a time-related manner. Neither Cu(II) nor the catechol alone induced any appreciable DNA cleavage. The reaction of SAL with Cu(II) was accompanied by the reduction of Cu(II) to Cu(I). Furthermore, SAL induced cell death in cultured PC12 cells which was exacerbated by Cu(II). From these data, it seems likely that SAL undergoes redox cycling catalyzed by Cu(II) to generate reactive species which may be responsible for the neurotoxic action of this catechol isoquinoline.",

author = "Kim, {Hyun Jung} and Yoon, {Hye Ran} and Stacy Washington and Chang, {In I.} and Oh, {Young J.} and Surh, {Young Joon}",

note = "Funding Information: This work was supported by the '96 Genetic Engineering Research Grant (to Y.-J.S.) from the Ministry of Education and in part by STEPI B-02-08-04 (to Y.J.O.), Republic of Korea.",

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AU - Yoon, Hye Ran

AU - Washington, Stacy

AU - Chang, In I.

AU - Oh, Young J.

AU - Surh, Young Joon

N1 - Funding Information: This work was supported by the '96 Genetic Engineering Research Grant (to Y.-J.S.) from the Ministry of Education and in part by STEPI B-02-08-04 (to Y.J.O.), Republic of Korea.

PY - 1997/12/5

Y1 - 1997/12/5

N2 - The naturally occurring neurotoxin, 1-methyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline (salsolinol; SAL), has been speculated to contribute to Parkinson's disease and neuropathology of chronic alcoholism. In the present study, we found the capability of SAL to cause DNA cleavage in the presence of Cu(II). Incubation of SAL and CuCl2 with calf thymus DNA caused strand breaks. Likewise, SAL in combination with Cu(II) mediated the strand scission in φX174 RFI supercoiled DNA in a time-related manner. Neither Cu(II) nor the catechol alone induced any appreciable DNA cleavage. The reaction of SAL with Cu(II) was accompanied by the reduction of Cu(II) to Cu(I). Furthermore, SAL induced cell death in cultured PC12 cells which was exacerbated by Cu(II). From these data, it seems likely that SAL undergoes redox cycling catalyzed by Cu(II) to generate reactive species which may be responsible for the neurotoxic action of this catechol isoquinoline.

AB - The naturally occurring neurotoxin, 1-methyl-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline (salsolinol; SAL), has been speculated to contribute to Parkinson's disease and neuropathology of chronic alcoholism. In the present study, we found the capability of SAL to cause DNA cleavage in the presence of Cu(II). Incubation of SAL and CuCl2 with calf thymus DNA caused strand breaks. Likewise, SAL in combination with Cu(II) mediated the strand scission in φX174 RFI supercoiled DNA in a time-related manner. Neither Cu(II) nor the catechol alone induced any appreciable DNA cleavage. The reaction of SAL with Cu(II) was accompanied by the reduction of Cu(II) to Cu(I). Furthermore, SAL induced cell death in cultured PC12 cells which was exacerbated by Cu(II). From these data, it seems likely that SAL undergoes redox cycling catalyzed by Cu(II) to generate reactive species which may be responsible for the neurotoxic action of this catechol isoquinoline.

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DNA strand scission and PC12 cell death induced by salsolinol and copper

Abstract

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