Para-phenylenediamine induced DNA damage and apoptosis through oxidative stress and enhanced caspase-8 and -9 activities in Mardin–Darby canine kidney cells

Chen, S.C.; Chen, Chaoran; Tioh, Y.L.; Zhong, Peng; Lin, Yi-Reng; Chye, Soi Moi

doi:10.1016/j.tiv.2010.02.011

Cited by 34 publications

(35 citation statements)

References 28 publications

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“…Several authors have shown that oxidative species induce DNA fragmentation as measured by the TUNEL assay [Ryu et al, 2003; Thomson et al, 2009; Chen et al, 2010], which is increased by MX [Taverna et al, 2001]. Accordingly, in this report we show DNA fragmentation in parasites treated with ROS/RNS species that increases vertically when MX is added simultaneously and maintained after the removal of the oxidative species.…”

Section: Discussionmentioning

confidence: 99%

DNA repair BER pathway inhibition increases cell death caused by oxidative DNA damage in Trypanosoma cruzi

et al. 2011

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Trypanosoma cruzi, a parasitic protozoan, is the etiological agent of Chagas disease, an endemic and neglected pathology in Latin America. It presents a life cycle that involves a hematophagous insect and man as well as domestic and wild mammals. The parasitic infection is not eliminated by the immune system of mammals; thus, the vertebrate host serves as a parasite reservoir. Additionally, chronic processes leading to dysfunction of the cardiac and digestive systems are observed. To establish a chronic infection some parasites should resist the oxidative damage to its DNA exerted by oxygen and nitrogen free radicals (ROS/RNS) generated in host cells. Till date there are no reports directly showing oxidative DNA damage and repair in T. cruzi. We establish that ROS/RNS generate nuclear and kinetoplastid DNA damage in T. cruzi that may be partially repaired by the parasite. Furthermore, we determined that both oxidative agents diminish T. cruzi cell viability. This effect is significantly augmented in parasites subsequently incubated with methoxyamine, a DNA base excision repair (BER) pathway inhibitor, strongly suggesting that the maintenance of T. cruzi viability is a consequence of DNA repair mechanisms.

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Section: Discussionmentioning

confidence: 99%

DNA repair BER pathway inhibition increases cell death caused by oxidative DNA damage in Trypanosoma cruzi

et al. 2011

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“…para ‐phenylenediamine ( p ‐PD) is used in manufacture of hair dyes, textile dyes, and leather dyes. Currently, p ‐PD is found in more than 1000 hair dye formulations and is the most frequently used hair dye component in Europe (Stanley et al, ; Chen et al, ). In Europe, North America, and Japan, more than one‐third of women use hair dyes, and permanent hair dyes account for three‐quarters of global use (Gago‐Dominguez et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…In Europe, North America, and Japan, more than one‐third of women use hair dyes, and permanent hair dyes account for three‐quarters of global use (Gago‐Dominguez et al, ). Epidemiological studies have found that women who used permanent hair dyes at least once a month have a higher risk of bladder cancer compared to non‐users (Gago‐Dominguez et al, ; Chen et al, ). Aside from personal use, professional hairdressers and textile dye industry workers are known to have frequent exposure to dyes containing p ‐PD.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis induced by para‐phenylenediamine involves formation of ROS and activation of p38 and JNK in chang liver cells

Chye

Tiong

Yip

et al. 2012

Environmental Toxicology

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para-Phenylenediamine (p-PD) is a suspected carcinogen, but it has been widely used as a component in permanent hair dyes. In this study, the mechanism of p-PD-induced cell death in normal Chang liver cells was investigated. The results demonstrated that p-PD decreased cell viability in a dose-dependent manner. Cell death via apoptosis was confirmed by enhanced DNA damage and increased cell number in the sub-G1 phase of the cell cycle, using Hoechst 33258 dye staining and flow cytometry analysis. Apoptosis via reactive oxygen species generation was detected by the dichlorofluorescin diacetate staining method. Mitogen-activated protein kinase (MAPK) activation was assessed by western blot analysis and revealed that p-PD activated not only stress-activated protein kinase (SAPK)/c-Jun N-terminal kinases (JNK) and p38 MAPK but also extracellular signal-regulated kinase (ERK). Cytotoxicity and apoptosis induced by p-PD were markedly enhanced by ERK activation and selectively inhibited by ERK inhibitor PD98059, thus indicating a negative role of ERK. In contrast, inhibition of p38 MAPK activity with the p38-specific inhibitor SB203580 moderately inhibited cytotoxicity and apoptosis induction by p-PD. Similarly, SP600125, an inhibitor of SAPK/JNK, moderately inhibited cytotoxicity and apoptosis induced by p-PD, thus implying that p38 MAPK and SAPK/JNK had a partial role in p-PD-induced apoptosis. Western blot analysis revealed that p-PD significantly increased phosphorylation of p38 and SAPK/JNK and decreased phosphorylation of ERK. In conclusion, the results demonstrated that SAPK/JNK and p38 cooperatively participate in apoptosis induced by p-PD and that a decreased ERK signal contributes to growth inhibition or apoptosis.

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“…Activation of caspase-3 is critical in genotoxicity-related apoptosis (Chen et al, 2010). Here, we examined the effect of satratoxin H on DNA damage by a micronucleus test, histone H2A phosphorylation (γH2AX) or an alkaline comet assay in PC12 cells.…”

Section: Satratoxin H Possessed Genotoxic Effectmentioning

confidence: 99%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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-Satratoxin H is an important air-and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that satratoxin H induced chromosome break. Also, satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of satratoxin H.

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Para-phenylenediamine induced DNA damage and apoptosis through oxidative stress and enhanced caspase-8 and -9 activities in Mardin–Darby canine kidney cells

Cited by 34 publications

References 28 publications

DNA repair BER pathway inhibition increases cell death caused by oxidative DNA damage in Trypanosoma cruzi

DNA repair BER pathway inhibition increases cell death caused by oxidative DNA damage in Trypanosoma cruzi

Apoptosis induced by para‐phenylenediamine involves formation of ROS and activation of p38 and JNK in chang liver cells

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

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