N-acetyl-l-cysteine prevents DNA damage induced by UVA, UVB and visible radiation in human fibroblasts

Morley, Nick; Curnow, Alison; Salter, Leo; Campbell, Sandra J.; Gould, David

doi:10.1016/j.jphotobiol.2003.06.004

Cited by 60 publications

(61 citation statements)

References 20 publications

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“…No significant loss of clonogenic survival in HPV-G cells was observed when cells were incubated with ICCM containing NAC in the priming phase for 24 h followed by ICCM only. NAC, a thiol-containing antioxidant, has been shown to protect cells against damage caused by ROS, although the exact ROS involved is currently unknown (34). Data from our laboratory have shown that bystander-induced cell death can be blocked in HPV-G cells incubated in ICCM containing NAC (35).…”

Section: Discussionmentioning

confidence: 94%

Modulation of Radiation Responses by Pre-exposure to Irradiated Cell Conditioned Medium

et al. 2007

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CitationModulation of radiation responses by pre-exposure to irradiated cell conditioned medium. The aim of this study was to investigate whether exposure of HPV-G cells to irradiated cell conditioned medium (ICCM) could induce an adaptive response if the cells were subsequently challenged with a higher ICCM dose. Clonogenic survival and major steps in the cascade leading to apoptosis, such as calcium influx and loss of mitochondrial membrane potential, were examined to determine whether these events could be modified by giving a priming dose of ICCM before the challenge dose. Clonogenic survival data indicated an ICCMinduced adaptive response in HPV-G cells ''primed'' with 5 mGy or 0.5 Gy ICCM for 24 h and then exposed to 0.5 Gy or 5 Gy ICCM. Reactive oxygen species (ROS) were found to be involved in the bystander-induced cell death. Calcium fluxes varied in magnitude across the exposed cell population, and a significant number of the primed HPV-G cells did not respond to the challenge ICCM dose. No significant loss of mitochondrial membrane potential was observed when HPV-G cells were exposed to 0.5 Gy ICCM for 24 h followed by exposure to 5 Gy ICCM for 6 h. Exposure of HPV-G cells to 5 mGy ICCM for 24 h followed by exposure to 0.5 Gy ICCM for 18 h caused a significant increase in mitochondrial mass and a change in mitochondrial location, events associated with the perpetuation of genomic instability. This study has shown that a priming dose of ICCM has the ability to induce an adaptive response in HPV-G cells subsequently exposed to a challenge dose of ICCM. ᭧

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Section: Discussionmentioning

confidence: 94%

Modulation of Radiation Responses by Pre-exposure to Irradiated Cell Conditioned Medium

et al. 2007

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“…We previously showed that L-NAC significantly reduced endothelin-induced increases in DNA synthesis in RASMC (7). A recent study also reported that L-NAC prevented DNA damage induced by ultraviolet A and visible radiation in human fibroblasts (14). However, D-NAC, which is known to be incapable of participating in GSH synthesis, was only half as effective as L-NAC in inhibiting topoisomerase-IIa activity, an enzyme involved in DNA synthesis as well as perturbing cell cycle progression through G2 (15).…”

Section: Of Nac Markedly Attenuated Ang Ii-induced [mentioning

confidence: 86%

Antioxidant Effects of Stereoisomers of N-Acetylcysteine (NAC), L-NAC and D-NAC, on Angiotensin II-Stimulated MAP Kinase Activation and Vascular Smooth Muscle Cell Proliferation

et al. 2004

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Abstract. We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang IIinduced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [ 3 H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC.

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“…5 In addition, several studies have demonstrated that an increase in antioxidant defense systems can reduce the deleterious effects of UV-induced ROS. The protective effects of non-enzymatic antioxidant or radical scavenger addition on UVB-, [18][19][20] UVA- 20 and UVA þ B- 21 induced damage have been reported. We have recently demonstrated that overexpression of CAT reduces UVB-induced apoptosis in human keratinocytes.…”

Section: Introductionmentioning

confidence: 99%

Protection of normal human reconstructed epidermis from UV by catalase overexpression

et al. 2006

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Reactive oxygen species (ROS) generated by ultraviolet (UV) irradiation are counterbalanced by endogenous antioxidant systems. To test the hypothesis of a novel photoprotective approach, we irradiated epidermis reconstructed with normal human keratinocytes overexpressing sustainably lentivirus-mediated catalase (CAT), copper/zinc superoxide dismutase (CuZnSOD) or manganese superoxide dismutase (MnSOD) enzymes. We found that following UVB irradiation there was a marked decrease in sunburn cell formation, caspase-3 activation and p53 accumulation in human reconstructed epidermis overexpressing CAT. Moreover, UVA-induced hypertrophy and DNA oxidation (8-oxodeoxyguanosine) were decreased by CAT overexpression. These effects were not achieved by overexpression of CuZnSOD or MnSOD. In conclusion, vector-mediated CAT overexpression could be a promising photoprotective tool against deleterious effects of UV irradiation such skin cancer especially in monogenic/polygenic photosensitive disorders characterized by ROS accumulation.

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N-acetyl-l-cysteine prevents DNA damage induced by UVA, UVB and visible radiation in human fibroblasts

Cited by 60 publications

References 20 publications

Modulation of Radiation Responses by Pre-exposure to Irradiated Cell Conditioned Medium

Modulation of Radiation Responses by Pre-exposure to Irradiated Cell Conditioned Medium

Antioxidant Effects of Stereoisomers of N-Acetylcysteine (NAC), L-NAC and D-NAC, on Angiotensin II-Stimulated MAP Kinase Activation and Vascular Smooth Muscle Cell Proliferation

Protection of normal human reconstructed epidermis from UV by catalase overexpression

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