State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi, Jiangsu 214122, P. R. China.
School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu 214122, China.
Food Funct. 2024 Sep 30;15(19):10110-10120. doi: 10.1039/d4fo02815e.
Lead (Pb) is a highly toxic metal with no physiological function in humans, accumulates in the body through food intake, and causes gut microbiome disorders and other hazards. In the present study, we examined the efficacy of a combination of chondroitin sulfate and CCFM8661 (CCFM8661 + CS) on tissue Pb accumulation and pathological damage to the liver and kidneys, gut microbiota, and fecal metabolites in Pb-exposed mice. Oral administration of CCFM8661 + CS to Pb-exposed mice reduced Pb accumulation in the liver, kidney, and bone tissues (from 3.70, 14.11 and 121.20 mg g wet tissue to 2.26, 8.72 and 65.57 mg g wet tissue, respectively) and increased total antioxidant capacity, superoxide dismutase, and glutathione in the liver and kidneys. Additionally, gut microbiome analysis showed that CCFM8661 + CS intervention attenuated Pb-induced perturbation in gut microbiota, altering the abundance of bacteria such as , , , and . Untargeted metabolomics analyses showed that CCFM8661 + CS significantly increased cinnamoylglycine, hippuric acid, and equol (to 31.24, 28.77 and 20.13 times the baseline, respectively) and decreased guanine and 4-coumaric acid (0.30 and 0.09 times the baseline, respectively) in the feces, affecting pathways such as purine and amino acid metabolism. Further analyses showed that promoting Pb excretion and restoring the Pb-impaired gut microbiome and its metabolism may be important contributors to CCFM8661 + CS alleviation of Pb toxicity.
铅（Pb）是一种剧毒金属，在人体中没有生理功能，通过食物摄入在体内积累，并导致肠道微生物组紊乱和其他危害。在本研究中，我们研究了硫酸软骨素和 CCFM8661（CCFM8661+CS）联合用药对暴露于 Pb 的小鼠组织中 Pb 积累和肝脏、肾脏的病理损伤、肠道微生物群和粪便代谢物的影响。给暴露于 Pb 的小鼠口服 CCFM8661+CS 降低了肝脏、肾脏和骨骼组织中的 Pb 积累（从 3.70、14.11 和 121.20mg/g 湿组织降至 2.26、8.72 和 65.57mg/g 湿组织），并增加了肝脏和肾脏中的总抗氧化能力、超氧化物歧化酶和谷胱甘肽。此外，肠道微生物组分析表明，CCFM8661+CS 干预减弱了 Pb 诱导的肠道微生物组失调，改变了细菌的丰度，如 、 、 、 。非靶向代谢组学分析表明，CCFM8661+CS 显著增加了肉桂酰甘氨酸、马尿酸和黄豆苷元（分别达到基线的 31.24、28.77 和 20.13 倍），降低了鸟嘌呤和 4-香豆酸（分别为基线的 0.30 和 0.09 倍），影响了嘌呤和氨基酸代谢等途径。进一步分析表明，促进 Pb 排泄和恢复 Pb 损伤的肠道微生物组及其代谢可能是 CCFM8661+CS 缓解 Pb 毒性的重要因素。
