This page lists medical journal articles discussing oxidative stress issues associated with Stachybotrys exposures.
The Health Effects of Stachybotrys Chartarum page of the Paradigm Change site provides further information on the effects of this toxic mold.
Nusuetrong P, Pengsuparp T, Meksuriyen D, Tanitsu M, Kikuchi H, Mizugaki M, Shimazu K, Oshima Y, Nakahata N, Yoshida M. Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells. Biological & pharmaceutical bulletin. 2008;31:1115–1120. PMID: 18520041
Satratoxin H caused apoptosis of PC12 cells within 24-h, as determined by DNA fragmentation and flow cytometric analysis. Satratoxin H increased reactive oxygen species (ROS) production and lipid peroxidation, as determined by malondialdehyde formation. These effects were attenuated by incubation of cells with GSH, suggesting that satratoxin H-induced increase in apoptosis of serum-deprived PC12 cells may be partially mediated through the generation of ROS.
Nusuetrong P, Yoshida M, Tanitsu MA, Kukuchi H, Mizugaki M, Shimazu K, Pengsuparp T, Meksuriyen D, Oshima Y, Nakahata N. Involvement of reactive oxygen species and stress-activated MAPKs in satratoxin H-induced apoptosis. European journal of pharmacology. 2005;507:239–246. PMID: 15659314
The study was undertaken to elucidate the mechanisms of the satratoxin H-induced cytotoxicity in PC12 cells. Satratoxin H caused cytotoxicity, which was reflected from apoptosis determined by chromatin staining and flow cytometry. Satratoxin H stimulated the phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). The data suggest that satratoxin H-induced apoptosis in PC12 cells is dependent on the activation of p38 MAPK/JNK and the increase in reactive oxygen species.
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