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. 2023 Feb 9;56(8):e13419. doi: 10.1111/cpr.13419

FIGURE 8.

FIGURE 8

Nicotinamide mononucleotide (NMN) recovers mitochondrial function and reduces oxidative stress in benzyl butyl phthalate (BBP)‐exposed mouse oocyte. (A) Germinal vesicle (GV) oocytes from each group were stained by Mito Tracker, and representative images of mitochondrial in control, BBP‐exposed and NMN + BBP oocytes. Red, Mitochondria. (B) BBP‐exposed oocytes displayed a significantly higher rate of the mis‐localized mitochondria than that in control oocytes, and NMN‐supplemented rescued the abnormal rate. Results are expressed as mean ± SD; experiments were repeated at least three times (NS, not significant; *p < 0.05; **p < 0.01; ***p < 0.001). (C) GV oocytes from each group were stained by JC‐1 to assess the mitochondrial membrane potential. The representative images of JC‐1 signal in control, BBP‐exposed and NMN + BBP oocytes. Red/green, JC‐1. (D) The ratio of red signal to green signal was significantly lower in BBP‐exposed oocytes than that in control oocytes, while NMN supplementation rescued this abnormality. (E) GV oocytes from each group were stained by dichlorofluorescein, and representative images of reactive oxygen species (ROS) signal in control, BBP‐exposed and NMN + BBP oocytes. Green, ROS. (F) BBP‐exposed oocytes appeared significantly higher ROS level than that in control oocytes, and NMN supplement recovered the ROS level after BBP exposure. Results are expressed as mean ± SD; experiments were repeated at least three times (NS, not significant; *p < 0.05; **p < 0.01; ***p < 0.001).