Abstract: 1-Octene-3-ol, a typical flavor substance of edible fungi, has been found to cause damage to the brain nervous system. In this work, we studied the neurotoxicity of different concentrations (0 (control group), 0.025% (volume fraction, the same below), 0.050%, 0.075%, 0.100%, 0.125%, 0.150%) of 1-octene-3-ol on HT22 cells through evaluation of apoptosis, oxidative stress, energy metabolism, and inflammation markers. The results showed that 1-octene-3-ol at a concentration above 0.050% significantly decreased the viability of HT22 cells, and caused a decrease in the mRNA expression of brain-derived neurotrophic factor (BDNF), thereby causing damage to the central nervous system. Moreover, apoptosis rates, the relative mRNA expression level of the apoptosis-regulating gene Bax/Bcl-2, reactive oxygen species (ROS) levels, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were increased, the mitochondrial membrane potential was decreased and cytochrome c oxidase concentration was increased. Besides, the relative mRNA expression levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 were also increased. These results indicated that 1-octene-3-ol mediated neurotoxic damage to HT22 cells through the co-regulation of the above aspects, which will provide a theoretical basis for studies on the neurotoxicity of 1-octene-3-ol.

Key words: 1-octene-3-ol; apoptosis; oxidative stress; inflammation; energy metabolism