Protection effect of taurine on nitrosative stress in the mice brain with chronic exposure to arsenic

Ma, Ning; Sasoh, Mikio; Kawanishi, Shosuke; Sugiura, Hirotsugu; Piao, Fengyuan

doi:10.1186/1423-0127-17-s1-s7

Cited by 40 publications

(15 citation statements)

References 73 publications

(63 reference statements)

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“…Furthermore, compared with temozolomide, bevacizumab and other expensive drugs, As 2 O 3 is an affordable drug with minimal economic concerns and can benefit the maximum number of GBM patients. A study in mice has demonstrated that As 2 O 3 is able to enter brain [ 44 ]. Although the infusion and efficiency of As 2 O 3 in human brain tumors remained to be further determined, it's likely that As 2 O 3 as a small molecular drug can pass through the blood brain barrier to inhibit GBM tumor growth by targeting GSCs in human brains.…”

Section: Discussionmentioning

confidence: 99%

Arsenic trioxide disrupts glioma stem cells via promoting PML degradation to inhibit tumor growth

et al. 2015

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Glioblastoma multiforme (GBM) is the most lethal brain tumor. Tumor relapse in GBM is inevitable despite maximal therapeutic interventions. Glioma stem cells (GSCs) have been found to be critical players in therapeutic resistance and tumor recurrence. Therapeutic drugs targeting GSCs may significantly improve GBM treatment. In this study, we demonstrated that arsenic trioxide (As2O3) effectively disrupted GSCs and inhibited tumor growth in the GSC-derived orthotopic xenografts by targeting the promyelocytic leukaemia (PML). As2O3 treatment induced rapid degradation of PML protein along with severe apoptosis in GSCs. Disruption of the endogenous PML recapitulated the inhibitory effects of As2O3 treatment on GSCs both in vitro and in orthotopic tumors. Importantly, As2O3 treatment dramatically reduced GSC population in the intracranial GBM xenografts and increased the survival of mice bearing the tumors. In addition, As2O3 treatment preferentially inhibited cell growth of GSCs but not matched non-stem tumor cells (NSTCs). Furthermore, As2O3 treatment or PML disruption potently diminished c-Myc protein levels through increased poly-ubiquitination and proteasome degradation of c-Myc. Our study indicated a potential implication of As2O3 in GBM treatment and highlighted the important role of PML/c-Myc axis in the maintenance of GSCs.

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Section: Discussionmentioning

confidence: 99%

Arsenic trioxide disrupts glioma stem cells via promoting PML degradation to inhibit tumor growth

et al. 2015

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“…Thus, 8-nitroguanine is a potentially mutagenic DNA lesion, which can participate in initiation and promotion in the infection-related carcinogenesis (Loeb & Preston, 1986;. Our studies have demonstrated that 8-nitroguanine is formed at the sites of carcinogenesis in humans and experimental animals (Ma et al, 2004;Pinlaor et al, 2004b;Ding et al, 2005;Horiike et al, 2005;Ma et al, 2006;Hoki et al, 2007a;Hoki et al, 2007b;Fujita et al, 2008;Ma et al, 2008;Tanaka et al, 2008;Ma et al, 2009;Ma et al, 2010). Moreover, our studies have demonstrated that 8-nitroguanine was formed in Oct3/4-positve stem cells in S. haematobium-associated cystitis and cancer tissues.…”

Section: Introductionmentioning

confidence: 75%

8-Nitroguanine, a Potential Biomarker to Evaluate the Risk of Inflammation-Related Carcinogenesis

Ma¹,

Murata²,

Ohnishi³

et al. 2012

Biomarker

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“…Such antidote effects of taurine or high capacity for taurine uptake into the cells (or conversely harmful effects of taurine depletion) have i.a . been found against alcohol (23–40), against the analgesic and fever-depressing drug acetaminophen (also called paracetamol) (41–44), against the aminoglycoside antibacterial drug gentamicin (45–47), against the immunosuppressant drug cyclosporine A (48, 49), against the anticancer drugs cisplatin (50–54), doxorubicin (also called adriamycin) (55–62), bleomycin (63–78), methotrexate (79) and taumustine (80), against the cytokine interleukin-2 (IL-2), which is used for immunotherapy of cancer (81–84), against the estrogen receptor modulator tamoxifen, which is used in therapy of breast cancer (85–87), against the antiarrhythmic drug amiodarone (88), against the beta -adrenergic agonists isoproterenol (55) and isoprenaline (89–92), against nicotine (93–95), against oxidized low-density lipoprotein (LDL) (96), against oxidized fish oil (97), against high glucose levels (96, 98–110), against fructose (111–122), against galactose (123), against advanced glycation end-products (AGEs) (100, 124, 125), against homocysteine (126–130), against the anti-inflammatory drugs ibuprofen (131) and indomethacin (132, 133), against the herbicide paraquat (65, 134, 135), against carbon tetrachloride (136–149), against menadione (150), against 1,4-naphtoquinone (137, 139), against hydrazine (137, 139), against trinitrobenzene sulfonic acid (151, 152), against acrylonitrile (153), against perchloroethylene (154), against methylene dianiline (155), against arsenic (156–164), against cadmium (…”

Section: Evidence Showing That Taurine Functions As a Biological Antimentioning

confidence: 99%

Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure.

Christophersen¹

2012

Microbial Ecology in Health & Disease

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There are several animal experiments showing that high doses of ionizing radiation lead to strongly enhanced leakage of taurine from damaged cells into the extracellular fluid, followed by enhanced urinary excretion. This radiation-induced taurine depletion can itself have various harmful effects (as will also be the case when taurine depletion is due to other causes, such as alcohol abuse or cancer therapy with cytotoxic drugs), but taurine supplementation has been shown to have radioprotective effects apparently going beyond what might be expected just as a consequence of correcting the harmful consequences of taurine deficiency per se. The mechanisms accounting for the radioprotective effects of taurine are, however, very incompletely understood. In this article an attempt is made to survey various mechanisms that potentially might be involved as parts of the explanation for the overall beneficial effect of high levels of taurine that has been found in experiments with animals or isolated cells exposed to high doses of ionizing radiation. It is proposed that taurine may have radioprotective effects by a combination of several mechanisms: (1) during the exposure to ionizing radiation by functioning as an antioxidant, but perhaps more because it counteracts the prooxidant catalytic effect of iron rather than functioning as an important scavenger of harmful molecules itself, (2) after the ionizing radiation exposure by helping to reduce the intensity of the post-traumatic inflammatory response, and thus reducing the extent of tissue damage that develops because of severe inflammation rather than as a direct effect of the ionizing radiation per se, (3) by functioning as a growth factor helping to enhance the growth rate of leukocytes and leukocyte progenitor cells and perhaps also of other rapidly proliferating cell types, such as enterocyte progenitor cells, which may be important for immunological recovery and perhaps also for rapid repair of various damaged tissues, especially in the intestines, and (4) by functioning as an antifibrogenic agent. A detailed discussion is given of possible mechanisms involved both in the antioxidant effects of taurine, in its anti-inflammatory effects and in its role as a growth factor for leukocytes and nerve cells, which might be closely related to its role as an osmolyte important for cellular volume regulation because of the close connection between cell volume regulation and the regulation of protein synthesis as well as cellular protein degradation. While taurine supplementation alone would be expected to exert a therapeutic effect far better than negligible in patients that have been exposed to high doses of ionizing radiation, it may on theoretical grounds be expected that much better results may be obtained by using taurine as part of a multifactorial treatment strategy, where it may interact synergistically with several other nutrients, hormones or other drugs for optimizing antioxidant protection and minimizing harmful posttraumatic inflammatory reactions, while using ...

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Protection effect of taurine on nitrosative stress in the mice brain with chronic exposure to arsenic

Cited by 40 publications

References 73 publications

Arsenic trioxide disrupts glioma stem cells via promoting PML degradation to inhibit tumor growth

Arsenic trioxide disrupts glioma stem cells via promoting PML degradation to inhibit tumor growth

8-Nitroguanine, a Potential Biomarker to Evaluate the Risk of Inflammation-Related Carcinogenesis

Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure.

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