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Chronic exposure to low-levels of organophosphate (OP) compounds, such as chlorpyrifos (CPF), induces oxidative stress and could be related to neurological disorders. Hydrogen has been identified as a novel antioxidant which could selectively scavenge hydroxyl radicals. We explore whether intake of hydrogen-rich water (HRW) can protect Wistar rats from CPF-induced neurotoxicity. Rats were gavaged daily with 6.75mg/kg body weight (1/20 LD50) of CPF and given HRW by oral intake. Nissl staining and electron microscopy results indicated that HRW intake had protective effects on the CPF-induced damage of hippocampal neurons and neuronal mitochondria. Immunostaining results showed that the increased glial fibrillary acidic protein (GFAP) expression in astrocytes induced by CPF exposure can be ameliorated by HRW intake. Moreover, HRW intake also attenuated CPF-induced oxidative stress as evidenced by enhanced level of MDA, accompanied by an increase in GSH level and SOD and CAT activity. Acetylcholinesterase (AChE) activity tests showed significant decrease in brain AChE activity after CPF exposure, and this effect can be ameliorated by HRW intake. An in vitro study demonstrated that AChE activity was more intense in HRW than in normal water with or without chlorpyrifos-oxon (CPO), the metabolically-activated form of CPF. These observations suggest that HRW intake can protect rats from CPF-induced neurotoxicity, and the protective effects of hydrogen may be mediated by regulating the oxidant and antioxidant status of rats. Furthermore, this work defines a novel mechanism of biological activity of hydrogen by directly increasing the AChE activity.

Background: To investigate the potential effects of molecular hydrogen on ovarian cancer.Methods: The in vivo study was performed using Hs38.T xenografted BALB/c nude mice. The mean tumor volume was monitored during 6 weeks of hydrogen inhalation. Immunohistochemistry (IHC) staining was performed to determine the Ki67 and CD34 expression. The in vitro effects of molecular hydrogen on proliferation of Hs38.T and PA-1 were determined by Cell Counting Kit (CCK)-8 assay. Matrigel invasion assay was performed to determine the cell invasion ability. Wounding assay was employed to examine the motile nature of ovarian cancer cells. Colony formation assay was performed to investigate the effect of molecular hydrogen in tumorigenicity. To further investigate the effects of molecular hydrogen on cancer stem cells (CSCs) properties, we performed sphere-formation assays. Results:The in vivo study demonstrated that 6 weeks of hydrogen inhalation significantly inhibited tumor growth, as evidenced by decreased mean tumor volume (32.30%) and Ki67 expression (30.00%). Hydrogen treatment decreased the expression of CD34 (74.00%) demonstrating its anti-angiogenesis effects. The in vitro study showed that hydrogen treatment significantly inhibits cancer cell proliferation, invasion, migration and colony formation both in Hs38.T and PA-1 cells. An important finding in this study was that molecular hydrogen could also markedly inhibit sphere-forming ability of both PA-1 and Hs38.T cells.Conclusions: Molecular hydrogen may exert anti-tumor role in ovarian cancer through suppressing the proliferation of CSCs-like cells and angiogenesis.

Organophosphate pesticides (OPs) are among the most widely used synthetic chemicals for the control of a wide variety of pests, and reactive oxygen species (ROS) caused by OPs may be involved in the toxicity of various pesticides. Previous studies have demonstrated that a reactivation of latent Epstein-Barr virus (EBV) could be induced by oxidative stress. In this study, we investigated whether OPs could reactivate EBV through ROS accumulation. The Raji cells were treated with chlorpyrifos (CPF), one of the most commonly used OPs. Oxidative stress indicators and the expression of the EBV immediate-early gene BZLF-1 were determined after CPF treatment. Our results show that CPF induces oxidative stress as evidenced by decreased malondialdehyde (MDA) level, accompanied by an increase in ROS production, DNA damage, glutathione (GSH) level, and superoxide dismutase (SOD) and catalase (CAT) activity. Moreover, CPF treatment significantly enhances the expression of BZLF-1, and the increased BZLF-1 expression was ameliorated by N-acetylcysteine (NAC) incubation. These results suggest that OPs could contribute to the reactivation of the EBV lytic cycle through ROS induction, a process that may play an important role in the development of EBV-associated diseases.