Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice — Toxicol Ind Health

: "Co-exposure of animals to ethanol and AFB1 showed additive effects on the activities of GST and CAT as well as on the GSH level. Histopathological study revealed that these compounds interact together to exacerbate their individual effects on the liver"

Read more: Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice — Toxicol Ind Health

The cap'n'collar transcription factor Nrf2 mediates both intrinsic resistance to environmental stressors and an adaptive response elicited by chemopreventive agents that determines susceptibility to electrophilic xenobiotics.

"Transcription factor Nrf2 regulates genes encoding drug-metabolising enzymes and drug transporters, as well as enzymes involved in the glutathione, thioredoxin and peroxiredoxin antioxidant pathways......."

Read more: CiteULike: The cap'n'collar transcription factor Nrf2 mediates both intrinsic resistance to environmental stressors and an adaptive response elicited by chemopreventive agents that determines susceptibility to electrophilic xenobiotics

Meth Labs, Wood Treatments, Pesticides and Ammonia Toxicity on Astrocytes~!

Astrocytes: (astroglia) : are characteristic star-shaped glial cells in the brain and spinal cord. They perform many functions, including biochemical support of endothelial cells which form the blood-brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a principal role in the repair and scarring process of the brain and spinal cord following traumatic injuries. (Wipedia: Astrocytes)

This study would suggest that any condition that impairs the antioxidant system which has a primary role in protecting astrocytes against damage (ie Nrf2)  would augment the toxicity of ammonia whether it be produced endogenously or from exogenous exposures. Young children, the elderly and those with impaired immune systems would also be more at risk. Products that contain ammonia or have it as an "inert" ingredient or exposures from hazardous environments such as methamphetamine labs pose an elevated risk for the above populations because they would be more susceptible to ammonia toxicity.

"This study demonstrated that in rats with HA or HE ammonia specifically promote GSH synthesis and export from astrocytes and increase its extracellular degradation, which may improve the availability of precursors for GSH synthesis in neurons and their resistance to ammonia toxicity."

Hilgier, W., Wegrzynowicz, M., Ruszkiewicz, J., Oja, S. S., Saransaari, P., and Albrecht, J. (2010). Direct exposure to ammonia and hyperammonemia increase the extracellular accumulation and degradation of astroglia-derived glutathione in the rat prefrontal cortex. Toxicological sciences : an official journal of the Society of Toxicology, 117(1):163-168. http://www.citeulike.org/user/HEIRS/article/7292948?show_msg=already_posted
 
 

Effects of exogenous GSH and methionine on methylation of inorganic arsenic in mice exposed to arsenite through drinking water.

"administration of GSH or methionine might potentiate the methylation capacity of arsenic in both liver and extrahepatic tissues, which may facilitate the excretion of arsenic and decrease arsenic related toxicities in the body."


"Jin, Y., Zhao, F., Zhong, Y., Yu, X., Sun, D., Liao, Y., Lv, X., Li, G., and Sun, G. (2010). Effects of exogenous gsh and methionine on methylation of inorganic arsenic in mice exposed to arsenite through drinking water. Environmental toxicology, 25(4):361-366."

CiteULike: Effects of exogenous GSH and methionine on methylation of inorganic arsenic in mice exposed to arsenite through drinking water.:

Ammonia and Hyperammonemia Increase the Extracellular Accumulation/ Degradation of Astroglia-Derived Glutathione.

These results suggest that in rats with HA or HE ammonia specifically promotes GSH synthesis and export from astrocytes and increases its extracellular degradation, which may improve the availability of precursors for GSH synthesis in neurons and their resistance to ammonia toxicity.

CiteULike: Direct Exposure to Ammonia and Hyperammonemia Increase the Extracellular Accumulation and Degradation of Astroglia-Derived Glutathione in the Rat Prefrontal Cortex: "Hilgier, W., Wegrzynowicz, M., Ruszkiewicz, J., Oja, S. S., Saransaari, P., and Albrecht, J. (2010). Direct exposure to ammonia and hyperammonemia increase the extracellular accumulation and degradation of astroglia-derived glutathione in the rat prefrontal cortex. Toxicol. Sci., pages kfq171+."

Methionine restriction up-regulates the expression of the pi class of glutathione S-transferase partially via the extracellular signal-regulated kinase-activator protein-1 signaling pathway initiated by glutathione depletion

Methionine restriction up-regulates the expression of the pi class of glutathione S-transferase partially via the extracellular signal-regulated kinase-activator protein-1 signaling pathway initiated by glutathione depletion: "URL: Methionine restriction up-regulates the expression of the pi class of glutathione S-transferase partially via the extracellular signal-regulated kinase-activator protein-1 signaling pathway initiated by glutathione depletion

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The Effect of Disruption of Genes for Peroxiredoxin-2, Glutathione Peroxidase-1 and Catalase on Erythrocyte Oxidative Metabolism.

The Effect of Disruption of Genes for Peroxiredoxin-2, Glutathione Peroxidase-1 and Catalase on Erythrocyte Oxidative Metabolism.: "URL: The Effect of Disruption of Genes for Peroxiredoxin-2, Glutathione Peroxidase-1 and Catalase on Erythrocyte Oxidative Metabolism.

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Check out some of our cool, more eco-friendly, non-toxic or got-to-have items in the HEIRS Web Store at Amazon or specialty items in our store at HEIRS Store Online.

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Glutathione depletion in nigrostriatal slice cultures: Gaba loss, dopamine resistance and protection by the tetrahydrobiopterin precursor sepiapterin

Gramsbergen, J. B. B., Sandberg, M., Møller Dall, A., Kornblit, B., and Zimmer, J. (2002). Glutathione depletion in nigrostriatal slice cultures: Gaba loss, dopamine resistance and protection by the tetrahydrobiopterin precursor sepiapterin. Brain research, 935(1-2):47-58. http://www.citeulike.org/user/HEIRS/article/6307660

Acetaminophen-Related Liver Damage May Be Prevented By Common Herbal Medicine

A well-known Eastern medicine supplement may help avoid the most common cause of liver transplantation, according to a study by researchers at the Stanford University School of Medicine.

LINK

Effect of sulforaphane on glutathione-adduct formation and on glutathione_s_transferase-dependent detoxification of acrylamide in caco-2 cells.

Summary: The data suggest that SFN might impair the GSH-dependent detoxification of AA by SFN-GSH adduct formation and, thus, lower the GSH concentrations available for its reaction with AA

Pernice, R., Hauder, J., Koehler, P., Vitaglione, P., Fogliano, V., and Somoza, V. (2009). Effect of sulforaphane on glutathione-adduct formation and on glutathione_s_transferase-dependent detoxification of acrylamide in caco-2 cells. Molecular Nutrition & Food Research, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6100240

Endogenous Peptide Protects Against Toxicants By Upregulating Nrf2/HO-1

Recent studies have shown that a peptide produced from thyroptropin-releasing hormone (TRH) in the hypothalamus called cyclo (His-Pro) (CHP) can provide neuroprotective effects against a number of toxicants including Paraquat, rotenone, glutamate and B-amyloid. The author determined that these effects are generated through the activation of Nrf2 and that the protective effects against Paraquat also involve HO-1. Knock-down of Nrf2 abolished these protective effects. Generally, the studies show evidence that CHP improves glutathione synthesis and prevented depletion and reduces the generation of ROS from these toxicants. Specifically, he notes that CHP is protective against H2O2 mediated apoptotic cell death. (Minelli) Paraquat exposure has been implicated as a risk factor for Parkinson's disease and having adverse effects on dopamine systems.

Other studies have shown that dopamine transmission is regulated by H2O2 and that H2O2 generated from respiring mitochondria are the major source of H2O2 neuronal signals. As we have noted, toxicants and other factors can lead to mitochondrial dysfunction which has been implicated in a number of health conditions including those commonly known as environmental illness. In the striatum, H2O2 controls dopamine release and it has been found that H2O2 inhibits dopamine release and activity through the activation of KATP channels.

Notes:

• 
  
  CHP is a substrate for OCT2 according to Taubert. Jonker explains that knock-down of OCT1 and OCT2 in the kidney can lead to an inhibition of excretion and excessive concentration of tetraethylammonium in the blood.  (Taubert, Jonker)

Kim Kramer
Health Education Information and Resource Services (HEIRS)
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