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.

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 102 quenchers could reduce the light-dependent toxicity of NR in C. reinhardtii, indicating that NR has a different mode of toxic action than RB.