FIGURE 1.

Acute hypobaric hypoxia caused formaldehyde (FA) accumulation and neurological deficits. (A) The time point of FA injection, intragastric administration of CoQ10, and hypobaric hypoxia exposure, as well as behavioral tests (D0: the hypobaric hypoxia exposure day). (B) Cerebral formaldehyde imaging using an in vivo small animal system with NaFA probe (λex/em = 440/550 nm). (C) Cerebral FA detection using QuantiChrom FA assay kit (p = 0.0044). (D–G) Neurological functions evaluated by open field test to show the total distance (p = 0.0004) (D), central distance (p = 0.0004) (E), latency to central entries (p < 0.0001) (F), and the frequency entering the center (p = 0.0001) (G) of each group on the first day after hypobaric hypoxia exposure. (H) Cognitive function evaluated by novel objective recognition (p = 0.0002) on the same day as open field test. Learning and memory ability assessed by step down test and showed the latency to electric shock (p = 0.0022) (I), and times of electric shock (p = 0.0468) (J) of each group on the second day after hypobaric hypoxia exposure. FA: formaldehyde; CoQ10: nano‐packed coenzyme Q10; sham: unexposed control group; HH: acute hypobaric hypoxia group. N = 6 in each group, with three independent experiments. Data are presented as mean ± SD; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001