Photosensitizers Neutral Red (Type I) and Rose Bengal (Type II) Cause Light-Dependent Toxicity in Chlamydomonas reinhardtii and Induce the Gpxh Gene via Increased Singlet Oxygen Formation

• Published in: Environmental science & technology 2004-12, Vol.38 (23), p.6307-6313
• Main Authors: Fischer, Beat B, Krieger-Liszkay, Anja, Eggen, Rik I. L
• Format: Article
• Language: English
• Subjects: Animal, plant and microbial ecology; Animals; Applied ecology; Biological and medical sciences; Chlamydomonas reinhardtii - drug effects; Chlamydomonas reinhardtii - metabolism; Dose-Response Relationship, Drug; Dose-Response Relationship, Radiation; Ecotoxicology, biological effects of pollution; Effects of pollution and side effects of pesticides on plants and fungi; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation - drug effects; Glutathione Peroxidase - genetics; Glutathione Peroxidase - metabolism; Histidine - metabolism; Light; Neutral Red - metabolism; Neutral Red - toxicity; Oxidative Stress - genetics; Oxidative Stress - radiation effects; Oxygen; Photosensitizing Agents - toxicity; Piperazines - metabolism; Rose Bengal - metabolism; Rose Bengal - toxicity; Singlet Oxygen - metabolism; Singlet Oxygen - radiation effects; Spinacia oleracea - chemistry; Spinacia oleracea - metabolism; Stress, Physiological - genetics; Thylakoids - chemistry; Thylakoids - metabolism; Toxicity; Up-Regulation - drug effects; Up-Regulation - radiation effects
• ISSN: 0013-936X; 1520-5851
• DOI: 10.1021/es049673y

The connection between the mode of toxic action and the genetic response caused by the type I photosensitizer and photosynthesis inhibitor neutral red (NR) and the type II photosensitizer rose bengal (RB) was investigated in the green alga Chlamydomonas reinhardtii. For both photosensitizers, a light intensity-dependent increase in toxicity and expression of the glutathione peroxidase homologous gene (Gpxh) was found. The toxicity of RB was reduced by the singlet oxygen (1O2) quenchers 1,4-diazabicyclo[2.2.2]octane and l-histidine, and the RB-induced Gpxh expression was stimulated in deuterium oxide-supplemented growth medium. These observations clearly indicate the involvement of 1O2 in both toxicity and the genetic response caused by RB. NR up-regulated the expression of typical oxidative and general stress response genes, probably by a type I mechanism, and also strongly induced the Gpxh expression. The stimulating effect of deuterium oxide in the growth medium suggested the involvement of 1O2 also in the NR-induced response. Indeed, an increased 1O2 formation was detected with EPR-spin trapping in NR-treated spinach thylakoids. However, none of the 1O2 quenchers could reduce the light-dependent toxicity of NR in C. reinhardtii, indicating that NR has a different mode of toxic action than RB.