Mutual synergistic toxicity between environmental toxicants: A study of mercury chloride and 4-nonylphenol

Lee, Seung Hwan; Cha, Mijin; Kang, Changkeun; Sohn, Eun-Tae; Lee, Hyunkyoung; Munawir, Al; Kim, Jong-Shu; Kim, Euikyung

doi:10.1016/j.etap.2008.08.009

Cited by 10 publications

(2 citation statements)

References 28 publications

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“…The addition of NP to the MWCNTs may have exacerbated the induction of intracellular ROS generation by simultaneously exerting adverse effects on the antioxidant defense system. Although studies have suggested that NP is an environmental contaminant that results in adverse environmental health effects attributable to oxidative stress both in vivo and in vitro [ 14 , 48 – 50 ], in our study, there were no significant differences in toxicity between the NP and CK groups. We inferred from these data that the NP exposure dose and time used in this study were not sufficient to stimulate ROS generation and induce oxidative damage; however, when NP adsorbs to MWCNTs, it remains in the tissues for a longer duration.…”

Section: Discussioncontrasting

confidence: 79%

Toxicological assessment of multi-walled carbon nanotubes combined with nonylphenol in male mice

et al. 2018

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Carbon nanotubes have attracted increasing attention attributable to their widespread application. To evaluate the joint toxicity of multi-walled carbon nanotubes (MWCNTs) and nonylphenol (NP), we investigated the toxicological effects of NP, pristine MWCNTs, and MWCNTs combined with NP in male mice. After exposing male mice by gavage for 5 days, intracellular superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, as well as malondialdehyde (MDA) and glutathione (GSH) levels in tissues were determined to evaluate in vivo oxidative stress. In addition, genotoxicity was assessed by examining DNA damage in mouse liver and sperm via the comet assay, and transmission electron microscopy (TEM) was used for direct visual observations of mitochondrial damage in the liver. Results from the oxidative damage and DNA damage experiments indicate that after adsorbing NP, MWCNTs at a high dose induce oxidative lesions in the liver and cause DNA damage in mouse sperm; these data offer new insights regarding the toxicological assessment of MWCNTs.

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Section: Discussioncontrasting

confidence: 79%

Toxicological assessment of multi-walled carbon nanotubes combined with nonylphenol in male mice

et al. 2018

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“…The synergistic activity of smoking with exposure to xenobiotics, such as arsenic, asbestos, and radon, in cancer risk is well known (Ahsan and Thomas 2004;Arnold and McLachlan 1996;Hassan et al 2007;Hays et al 2006;IARC 2004;Lee et al 2009). The mechanism is thought to operate through the CYP enzymes, especially CYP1A2, which takes part in the activation of carcinogens (Nishikawa et al 2004).…”

Section: Cigarette Smokementioning

confidence: 99%

Lung Cancer and Environmental Chemical Exposure: A Review of Our Current State of Knowledge With Reference to the Role of Hormones and Hormone Receptors as an Increased Risk Factor for Developing Lung Cancer in Man

et al. 2010

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Lung cancer is a dominant cause of cancer mortality. The etiology of lung cancer is mainly related to cigarette smoking, airborne genotoxic carcinogens, and arsenic, but its sex-specific incidence suggests that other mechanisms, such as hormones, may also be involved in the process of carcinogenesis. A number of agents commonly present in the living environment can have dual biological effects: not only are they genotoxic / carcinogenic, but they are also hormonally active as xenoestrogens. This dualism may explain sex-specific differences reported in both types and incidence of lung cancer. In a novel approach to investigate the complexity of lung cancer, etiology, including systems biology, will be used as a tool for a simultaneous interpretation of measurable environmental and biological parameters. Using this approach, the etiology of human lung cancer can be more thoroughly investigated using the available data from oncology and environmental health. The information gained could be applied in the introduction of preventive measures, in personalized medicine, and in more relevant legislation, which should be adjusted to reflect the current knowledge on the complex environmental interactions underlying this life-threatening disease.

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Modulation of mercury-induced mitochondria-dependent apoptosis by glycine in hepatocytes

Pal

Das

et al. 2011

Amino Acids

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Mercury (Hg) is one of the universal environmental pollutants and is responsible for various organ pathophysiology including oxidative stress-induced hepatic disorders. In the present study, we aimed to explore the protective role of glycine in Hg-induced cytotoxicity and cell death in murine hepatocytes. Exposure of mercury (20 μM), in the form HgCl2 for 1 h, significantly enhanced the ALT and ALP leakage, increased reactive oxygen species production, reduced cell viability and distorted the antioxidant status of hepatocytes. Flow cytometric analyses shows that Hg-induced apoptotic death in hepatocytes. Mechanism of this pathophysiology involves reduced mitochondrial membrane potential, variations in Bcl-2/Bad proteins, activation of caspases and cleavage of PARP protein. In addition, Hg distinctly increased NF-κB phosphorylation in association with IKKα phosphorylation and IκBα degradation. Concurrent treatment with glycine (45 mM), however, reduced Hg-induced oxidative stress, attenuated the changes in NF-κB phosphorylation and protects hepatocytes from Hg-induced apoptotic death. Hg also distinctly increased the phosphorylation of p38, JNK and ERK mitogen-activated protein kinase (MAPKs). Glycine treatment suppressed these apoptotic events, signifying its protective role in Hg-induced hepatocyte apoptosis as referred by reduction of p38, JNK and ERK MAPK signaling pathways. Results suggest that glycine can modulate Hg-induced oxidative stress and apoptosis in hepatocytes probably because of its antioxidant activity and functioning via mitochondria-dependent pathways and could be a beneficial agent in oxidative stress-mediated liver diseases.

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Mutual synergistic toxicity between environmental toxicants: A study of mercury chloride and 4-nonylphenol

Cited by 10 publications

References 28 publications

Toxicological assessment of multi-walled carbon nanotubes combined with nonylphenol in male mice

Toxicological assessment of multi-walled carbon nanotubes combined with nonylphenol in male mice

Lung Cancer and Environmental Chemical Exposure: A Review of Our Current State of Knowledge With Reference to the Role of Hormones and Hormone Receptors as an Increased Risk Factor for Developing Lung Cancer in Man

Modulation of mercury-induced mitochondria-dependent apoptosis by glycine in hepatocytes

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