Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, China.
Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Front Endocrinol (Lausanne). 2022 Jul 13;13:937281. doi: 10.3389/fendo.2022.937281. eCollection 2022.
Benzene is a ubiquitous pollutant and mainly accumulates in adipose tissue which has important roles in metabolic diseases. The latest studies reported that benzene exposure was associated with many metabolic disorders, while the effect of benzene exposure on adipose tissue remains unclear. We sought to investigate the effect using and experiments. Male adult C57BL/6J mice were exposed to benzene at 0, 1, 10 and 100 mg/kg body weight by intragastric gavage for 4 weeks. Mature adipocytes from 3T3-L1 cells were exposed to hydroquinone (HQ) at 0, 1, 5 and 25 μM for 24 hours. Besides the routine hematotoxicity, animal experiments also displayed significant body fat content decrease from 1 mg/kg. Interestingly, the circulating non-esterified fatty acid (NEFA) level increased from the lowest dose < 0.05). Subsequent analysis indicated that body fat content decrease may be due to atrophy of white adipose tissue (WAT) upon benzene exposure. The average adipocyte area of WAT decreased significantly even from 1 mg/kg with no significant changes in total number of adipocytes. The percentages of small and large adipocytes in WAT began to significantly increase or decrease from 1 mg/kg (all < 0.05), respectively. Critical genes involved in lipogenesis and lipolysis were dysregulated, which may account for the disruption of lipid homeostasis. The endocrine function of WAT was also disordered, manifested as significant decrease in adipokine levels, especially the leptin. cell experiments displayed similar findings in decreased fat content, dysregulated critical lipid metabolism genes, and disturbed endocrine function of adipocytes after HQ treatment. Pearson correlation analysis showed positive correlations between white blood cell (WBC) count with WAT fat content and plasma leptin level ( = 0.330, 0.344, both < 0.05). This study shed light on the novel aspect that benzene exposure could induce lipodystrophy and disturb endocrine function of WAT, and the altered physiology of WAT might in turn affect benzene-induced hematotoxicity and metabolic disorders. The study provided new insight into understanding benzene-induced toxicity and the relationship between benzene and adipose tissue.
苯是一种普遍存在的污染物，主要积聚在脂肪组织中，而脂肪组织在代谢疾病中起着重要作用。最新的研究报告称，苯暴露与许多代谢紊乱有关，而苯暴露对脂肪组织的影响尚不清楚。我们试图通过 和 实验来研究其影响。雄性成年 C57BL/6J 小鼠通过灌胃暴露于 0、1、10 和 100 mg/kg 体重的苯 4 周。3T3-L1 细胞中的成熟脂肪细胞用对苯二酚（HQ）在 0、1、5 和 25 μM 下暴露 24 小时。除了常规的血液毒性外，动物实验还显示出显著的体脂含量下降，从 1 mg/kg 开始（ < 0.05）。有趣的是，循环非酯化脂肪酸（NEFA）水平从最低剂量开始增加 < 0.05）。随后的分析表明，体脂含量的下降可能是由于苯暴露导致白色脂肪组织（WAT）萎缩。WAT 的平均脂肪细胞面积从 1 mg/kg 开始显著减小，而脂肪细胞总数没有明显变化。WAT 中小和大脂肪细胞的百分比从 1 mg/kg 开始显著增加或减少（均 < 0.05）。参与脂肪生成和脂肪分解的关键基因失调，可能导致脂质稳态的破坏。WAT 的内分泌功能也失调，表现为脂肪因子水平显著下降，尤其是瘦素。HQ 处理后的细胞实验也显示出脂肪含量下降、关键脂质代谢基因失调以及脂肪细胞内分泌功能紊乱的类似发现。Pearson 相关分析显示，白细胞（WBC）计数与 WAT 脂肪含量和血浆瘦素水平呈正相关（ = 0.330，0.344，均 < 0.05）。本研究揭示了苯暴露可引起脂肪营养不良并扰乱 WAT 的内分泌功能的新方面，而 WAT 的改变生理学可能反过来影响苯诱导的血液毒性和代谢紊乱。该研究为理解苯诱导的毒性和苯与脂肪组织之间的关系提供了新的见解。
