Saad Muhamad Fikri Shazlan, Abdullah Muhammad Nazrul Hakim, Lim Vuanghao, Bahari Hasnah, Khoo Boon Yin, Tan Jun Jie, Yong Yoke Keong
Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.
Toxicol Appl Pharmacol. 2025 Feb;495:117227. doi: 10.1016/j.taap.2025.117227. Epub 2025 Jan 7.
Bisphenol A (BPA), an endocrine disruptor, is linked to cancer progression in estrogen-responsive tissues, but its role in promoting colorectal cancer (CRC) progression in the context of obesity remains underexplored. This study examines BPA's influence on CRC in obese Sprague-Dawley rats using network toxicology and experimental models. Computational analysis using the Database for Annotation, Visualization, and Integrated Discovery identified pathways such as "CRC" and "chemical carcinogenesis-receptor activation", implicating the PI3K-AKT pathway in IL-1 beta upregulation and BPA's role in CRC during obesity. Thirty male rats were grouped (n = 6) as follows: N (normal diet), NC (normal diet + CRC), HC (high-fat diet + CRC), NCB (normal diet + CRC + BPA), and HCB (high-fat diet + CRC + BPA). CRC was induced with 1,2-dimethylhydrazine (40 mg/kg), and BPA (25 mg/kg) was administered for 19 weeks. Although BPA exposure did not affect body weight or biochemical parameters, the HCB group exhibited significant histopathological changes in the colon, including lymphoid hyperplasia, liver damage, and increased IL-1β levels. Furthermore, diet influenced adipocyte size, exacerbating BPA's effects on CRC progression. Findings suggest BPA may worsen CRC progression in obese rats through identified pathways, promoting multi-organ pathology and underscoring the need for stricter regulations, especially for vulnerable populations. ENVIRONMENTAL IMPLICATION: Bisphenol A (BPA), a widespread environmental contaminant, is increasingly linked to serious health issues, including cancer, in susceptible populations. Our study highlights BPA's role in promoting obesity-driven colorectal cancer (CRC) progression, demonstrating its carcinogenic potential in high-risk contexts. These findings emphasize the urgent need for regulatory scrutiny of BPA exposure, particularly in obese individuals, and support the development of safer alternatives. Addressing BPA's impact can contribute to preventive health strategies and inform policies aimed at reducing environmental and public health risks associated with endocrine-disrupting chemicals.
双酚A(BPA)是一种内分泌干扰物,与雌激素反应性组织中的癌症进展有关,但其在肥胖背景下促进结直肠癌(CRC)进展中的作用仍未得到充分研究。本研究使用网络毒理学和实验模型,研究了BPA对肥胖的斯普拉格-道利大鼠结直肠癌的影响。使用注释、可视化和综合发现数据库进行的计算分析确定了“结直肠癌”和“化学致癌作用-受体激活”等途径,表明PI3K-AKT途径参与白细胞介素-1β上调以及肥胖期间BPA在结直肠癌中的作用。将30只雄性大鼠分为以下几组(n = 6):N(正常饮食)、NC(正常饮食+结直肠癌)、HC(高脂饮食+结直肠癌)、NCB(正常饮食+结直肠癌+BPA)和HCB(高脂饮食+结直肠癌+BPA)。用1,2-二甲基肼(40 mg/kg)诱导结直肠癌,并给予BPA(25 mg/kg),持续19周。虽然BPA暴露不影响体重或生化参数,但HCB组在结肠中表现出显著的组织病理学变化,包括淋巴组织增生、肝脏损伤和白细胞介素-1β水平升高。此外,饮食影响脂肪细胞大小,加剧了BPA对结直肠癌进展的影响。研究结果表明,BPA可能通过已确定的途径使肥胖大鼠的结直肠癌进展恶化,促进多器官病变,并强调需要更严格的监管,特别是对易感人群。环境影响:双酚A(BPA)是一种广泛存在的环境污染物,在易感人群中越来越多地与包括癌症在内的严重健康问题相关联。我们的研究突出了BPA在促进肥胖驱动的结直肠癌(CRC)进展中的作用,证明了其在高风险情况下的致癌潜力。这些发现强调了对BPA暴露进行监管审查的迫切需要,特别是在肥胖个体中,并支持开发更安全的替代品。解决BPA的影响有助于预防健康策略,并为旨在降低与内分泌干扰化学物质相关的环境和公共健康风险的政策提供信息。