Fig. 1: Effects of nicotine exposure and its cessation on sperm and testes. | Communications Biology

Fig. 1: Effects of nicotine exposure and its cessation on sperm and testes.

From: Mechanisms and reversibility of nicotine-induced spermatogenesis impairment and DNA methylation changes

Fig. 1

A–D Sperm characteristics in non-smokers (n = 18; Control), smokers (n = 19; Smoking), and ex-smokers (n = 14; Cessation). A Sperm concentration. B Total motility. C Progressive motility. D Rate of normal morphology. E Schematic diagram illustrating experimental design and animal group allocation. F–I Dynamical parameters of sperm samples from three mice groups (CON, NIC, and CES) were measured by Computer-assisted sperm analysis (CASA, n = 8 mice per group). F Sperm concentration. G Sperm motility. H Progressive motility. I Average path velocity (VAP). J, K testicular length (J, n = 22 testes per group) and weight (K, n = 10 mice per group) in NIC mice relative to CON and CES mice. L Hematoxylin and eosin (H&E) staining of testicular samples from three groups post-nicotine exposure. Black scale bar = 200 μm, blue scale bar = 40 μm. M, N Histological characteristics of seminiferous tubule examined by H&E staining. M Spermatogenic epithelium thickness (n = 20 tubules per group). N Seminiferous tubule diameter (n = 24 tubules per group). O Plasma concentrations of testosterone (n = 8 mice per group). Data are represented as mean ± SEM. All statistical analyses were performed using ANOVA followed by Bonferroni’s multiple comparisons test, ****p < 0.0001; ***p < 0.001; **p < 0.01; *p < 0.05; ns not significant.

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