Cited by 90Cell death mechanisms and regulationRedox biology and oxidative stressAntioxidant Activity and Oxidative Stress

Cells Preconditioned with Mild, Transient UVA Irradiation Acquire Resistance to Oxidative Stress and UVA-induced Apoptosis

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Yang, Yusong, Sharma, Abha, Sharma, Rajendra, Patrick, Brad, Singhal, Sharad S., Zimniak, Piotr, Awasthi, Sanjay, Awasthi, Yogesh C.·2003·Journal of Biological Chemistry

Abstract

Because 4-hydroxynonenal (4-HNE) has been suggested to be involved in oxidative stress-mediated apoptosis (Cheng, J. Z., Sharma, R., Yang, Y., Singhal, S. S., Sharma, A., Saini, M. K., Singh, S. V., Zimniak, P., Awasthi, S., and Awasthi, Y. C. (2001) J. Biol. Chem. 276, 41213-41223) and UVA irradiation also causes lipid peroxidation, we have examined the role of 4-HNE in UVA-mediated apoptosis. K562 cells irradiated with UVA (3.0 milliwatts/cm2) for 5, 15, and 30 min showed a time dependent increase in 4-HNE levels. As judged by the activation of caspases, apoptosis was observed only in cells irradiated for 30 min. Within 2 h of recovery in normal medium, 4-HNE levels in 5 and 15 min UVA, irradiated cells returned to the basal or even lower levels but in cells irradiated for 30 min, 4-HNE levels remained consistently higher. The cells irradiated with UVA for 5 min and allowed to recover for 2 h in normal medium (UVA-preconditioned cells) showed a remarkable induction of hGST5.8, which catalyzes conjugation of 4-HNE to glutathione (GSH), and RLIP76 (Ral BP-1), which mediates the transport of the conjugate, GS-HNE. In cells irradiated with UVA for 30 min the induction of RLIP76 or hGST5.8 was not observed. The preconditioned cells transported GS-HNE into the medium at a rate about 2-fold higher than the controls and the transport was inhibited (65%) by coating the cells with anti-RLIP76 IgG. Upon treatment with xanthine/xanthine oxidase (XA/XO), 4-HNE, or prolonged UVA exposure, the control cells showed a sustained activation of c-Jun N-terminal kinase (JNK) and apoptosis. However, in the UVA-preconditioned cells, apoptosis was not observed, and JNK activation was inhibited. This resistance of preconditioned cells to XA/XO-, 4-HNE-, or UVA-induced apoptosis could be abrogated when these cells were coated with anti-RLIP76 IgG to block the efflux of GS-HNE. These studies strongly suggest a role of 4-HNE in UVA-mediated apoptosis.

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Crossref · 10.1074/jbc.m305766200

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  • Rlip is a stress-protective ATPase of the mercapturic acid pathway that couples clathrin-dependent endocytosis with the efflux of glutathione-electrophile conjugates.

    “Rlip is a stress-protective ATPase of the mercapturic acid pathway that couples clathrin-dependent endocytosis with the efflux of glutathione–electrophile conjugates.”

    From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [2]

    The paper describes RLIP76 as mediating ATP-dependent efflux of the glutathione conjugate GS-HNE (opening passage; page unavailable). Its Results also link RLIP76-mediated efflux to resistance against 4-HNE-induced apoptosis in UVA-preconditioned cells. Our copy does not describe RLIP76 as part of the mercapturic acid pathway or say that it couples this efflux to clathrin-dependent endocytosis. (LLM, conf=0.88)

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  1. Pourzand, C., Watkin, R. D., Brown, J. E., and Tyrrell, R. M. (1999) Proc. Natl. Acad. Sci. U. S. A. 96, 6751-6756
  2. Hatchard, C. G., and Parker, C. A. (1956) Proc. R. Soc. London, Ser. A. 235, 518
  3. Towbin, H., Staehelin, T., and Gordon, J. (1979) Proc. Natl. Acad. Sci. U. S. A. 76, 4350 -4354
  4. Yoritaka, A., Hattori, N., Uchida, K., Tanaka, M., Stadtman, E. R., and Mizuno, Y. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 2696 -2701

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Authors
Yang, Y., Sharma, A., Sharma, R., Patrick, B., Singhal, S. S., Zimniak, P., Awasthi, S., & Awasthi, Y. C.
Affiliations
  • The University of Texas Medical Branch at Galveston (US)
  • The University of Texas at Arlington (US)
  • Central Arkansas Veterans Healthcare System (US)
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-10
Volume
278
Issue
42
Pages
41380-41388
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2081110896
Cited by
90
References
2
Citations by year
2023: 1 · 2022: 1 · 2021: 7 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 6 · 2012: 4
FWCI
3.75
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (EY 04396)
  • National Eye Institute (EY-04396)
  • National Cancer Institute (CA 77495, R01CA077495)
  • National Institute of General Medical Sciences (GM-32304, R01GM032304)
  • National Institute of Environmental Health Sciences (ES 07804, R01ES007804)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
UVA irradiation, apoptosis resistance, oxidative stress, 4-hydroxynonenal, lipid peroxidation, preconditioning, K562 cells, RLIP76, glutathione conjugation, JNK activation, xanthine/xanthine oxidase, caspase activation, cell survival signaling
MeSH terms
Aldehydes, Biological Transport, Dose-Response Relationship, Radiation, Glutathione, Glutathione Transferase, Growth Inhibitors, Humans, Microscopy, Fluorescence, Time Factors, Ultraviolet Rays, Xanthine Oxidase, Blotting, Western, Signal Transduction, Cysteine Proteinase Inhibitors, Apoptosis, Oxidative Stress, K562 Cells, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases

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