Alabi Okunola A, Ologbonjaye Kehinde I, Sorungbe Adewale A, Shokunbi Olutayo S, Omotunwase Oyinkansola I, Lawanson Gbemisola, Ayodele Oluwafemi G
Department of Biology, Federal University of Technology, Akure, Ondo State, Nigeria.
Department of Biochemistry, School of Basic Medical Sciences, Babcock University, Ilishan-Remo, Ogun State, Nigeria.
J Health Pollut. 2021 Feb 25;11(29):210307. doi: 10.5696/2156-9614-11.29.210307. eCollection 2021 Mar.
Bisphenol A (BPA) is known to alter sperm morphology, but information is limited on the most susceptible stage(s) of spermatogenesis, especially in mice.
This study investigated the reproductive, biochemical, and hematological changes caused by exposure to BPA in male albino mice. The genotoxicity of BPA to the six stages of spermatogenesis in mice was determined.
Mice were exposed orally to BPA at 0.5, 1.0, 2.0, and 5.0 mg/kg bw doses for 5 days and assessed for sperm morphology after 35 days. Based on the result, the second group of mice was exposed to BPA at 1.0 mg/kg bw dose for 5 days, their spermatozoa were assessed for sperm morphology based on BPA exposure at the 6 maturation stages of spermatogenesis: spermatozoa, elongating spermatids, round spermatids, secondary spermatocytes, primary spermatocytes, and spermatogonia. Biochemical and hematological analyses of the blood of exposed mice were also carried out.
The results showed that BPA induced concentration-dependent, significantly (p<0.05) increased sperm cell abnormalities at three of the four concentrations tested, with the exception of 0.5 mg/kg bw, in comparison with the negative control. The highest frequency of sperm aberrations was induced in spermatozoa exposed to BPA while at the primary spermatocytes. The order of induced sperm abnormality at the different stages of exposure was: primary spermatocytes > elongating spermatids > spermatozoa > spermatogonia > round spermatids > secondary spermatocytes. The results of the biochemical analysis showed significantly (p<0.05) increased serum urea, creatinine, and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with a concomitant decrease in total protein content at the various stages of spermatogenesis. In addition, the results for hematological parameters showed several significant (p<0.05) modulations in mice exposed to BPA.
These data showed that BPA is most toxic to primary spermatocytes and alterations of biochemical and hematological parameters might be the mechanisms of induced toxicity.
The Research Ethics Committee, Federal University of Technology, Akure approved the study protocols.
The authors declare no competing financial interests.
已知双酚A（BPA）会改变精子形态，但关于精子发生最敏感阶段的信息有限，尤其是在小鼠中。
本研究调查了雄性白化小鼠暴露于双酚A后引起的生殖、生化和血液学变化。确定了双酚A对小鼠精子发生六个阶段的遗传毒性。
将小鼠以0.5、1.0、2.0和5.0 mg/kg体重的剂量口服暴露于双酚A 5天，并在35天后评估精子形态。根据结果，第二组小鼠以1.0 mg/kg体重的剂量暴露于双酚A 5天，根据精子发生的6个成熟阶段（精子、伸长型精子细胞、圆形精子细胞、次级精母细胞、初级精母细胞和精原细胞）的双酚A暴露情况评估其精子形态。还对暴露小鼠的血液进行了生化和血液学分析。
结果显示，与阴性对照相比，在测试的四种浓度中的三种浓度下，双酚A诱导了浓度依赖性的、显著（p<0.05）增加的精子细胞异常，0.5 mg/kg体重的浓度除外。在暴露于双酚A的精子和初级精母细胞中诱导的精子畸变频率最高。在不同暴露阶段诱导精子异常的顺序为：初级精母细胞>伸长型精子细胞>精子>精原细胞>圆形精子细胞>次级精母细胞。生化分析结果显示，在精子发生的各个阶段，血清尿素、肌酐、丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）活性显著（p<0.05）增加，同时总蛋白含量降低。此外，血液学参数结果显示，暴露于双酚A的小鼠有几个显著（p<0.05）的变化。
这些数据表明，双酚A对初级精母细胞毒性最大，生化和血液学参数的改变可能是诱导毒性的机制。
阿库雷联邦理工大学研究伦理委员会批准了研究方案。
作者声明不存在相互竞争的财务利益。
