To investigate the regulatory effect of lactic acid bacteria on the toxicity by perfluorooctane sulfonate (PFOS) in mice and its possible mechanism, 36 male C57BL/6J mice were randomized into six groups. The control group and the PFOS model group were treated with 30 g/L (sucrose) solution, while the four strain intervention groups (Lactobacillus bulgaricus D2A49, Lactobacillus bulgaricus DQHXNS3L9, Pediococcus pentosaceus FFSCDJY63L2 and Pediococcus pentosaceus JSNJPK1-1) were treated with lactic acid bacteria resuspended in 30 g/L(sucrose) solution for 30 days (109 CFU/mL). From day 16 to 30, the PFOS model group and the strain intervention groups were exposed with 3 μg/(g BW·d) PFOS. Liver parameters such as liver index, IL-1β, TNF-α and serum liver enzymes levels were determined; histopathological analysis was performed for liver and colon; the levels of IL-10, TNF-α and the tight junction protein in colon and short-chain fatty acids in faces were also examined. The results indicated that PFOS exposed mice developed hallmark features of liver and intestinal damage, and lactic acid bacteria attenuated the development of the damage. Further analysis demonstrated that supplementation with L. bulgricus DQHXNS3L9 and L. bulgricus D2A49 significantly decreased the liver index, serum liver enzyme content and intestine inflammation, attenuated the pathological changes in liver and colon tissues, and elevated the level of the tight junction protein in colon and short-chain fatty acids in stool. Therefore, lactic acid bacteria showed the capabilities in preventing and alleviating liver and intestinal damage caused by PFOS exposure through short-chain fatty acids regulation with individual differences.
SUN Shanshan
,
WU Xiaobing
,
YANG Shurong
,
JIAO Ting
,
SI Qian
,
WANG Gang
,
ZHAO Jianxin
,
ZHANG Hao
,
CHEN Wei
. Lactic acid bacteria relieve liver and intestinal damage caused by perfluorooctane sulfonate exposure[J]. Food and Fermentation Industries, 2020
, 46(16)
: 17
-23
.
DOI: 10.13995/j.cnki.11-1802/ts.023972
[1] 宋彦敏,周连宁,郝文龙,等.全氟化合物的污染现状及国内外研究进展[J]. 环境工程,2017,35(10):82-86.
[2] TOMY G T, BUDAKOWSKI W, HALLDORSON T, et al. Fluorinated organic compounds in an eastern Arctic marine food web[J]. Environmental science & technology, 2004, 38(24):6 475-6 481.
[3] XU C, JIANG Z Y, LIU Q, et al. Estrogen receptor beta mediates hepatotoxicity induced by perfluorooctane sulfonate in mouse[J]. Environmental Science and Pollution Research, 2017, 24(15): 13 414-13 423.
[4] MARTIN M T, BRENNAN R J, HU W Y, et al. Toxicogenomic study of triazole fungicides and perfluoroalkyl acids in rat livers predicts toxicity and categorizes chemicals based on mechanisms of toxicity[J]. Toxicological Sciences, 2007, 97(2):595-613.
[5] CHEN X, NIE X, MAO J, et al. Perfluorooctanesulfonate induces neuroinflammation through the secretion of TNF-α mediated by the JAK2/STAT3 pathway[J]. NeuroToxicology, 2018, 66(3): 32-42.
[6] LONG M,KJELDSEN L,GHISARI M,et al. Endocrine disrupting compounds and heavy metals in the amniotic fluid and neurodevelopment disorders: A case-control study[J]. Toxicology Letters, 2014, 229(S1): 121.
[7] WANG H X,DU H Y,YANG J Q,et al. PFOS, PFOA, estrogen homeostasis, and birth size in Chinese infants[J]. Chemosphere, 2019, 221(4): 349-355.
[8] HAUGHOM B, ØYSTEIN S.The mechanism underlying the hypolipemic effect of perfluorooctanoic acid (PFOA), perfluorooctane sulphonic acid (PFOSA) and clofibric acid[J]. Biochimica et Biophysica Acta(BBA)-Lipids and Lipid Metabolism, 1992, 1 128(1):65-72.
[9] CHRISTENSEN K Y, RAYMOND M, MEIMAN J. Perfluoroalkyl substances and metabolic syndrome[J]. International Journal of Hygiene and Environmental Health, 2019, 222(1):147-153.
[10] DEE G S,JIE X,ANOO P S. Positive association between perfluoroalkyl chemicals and hyperuricemia in children[J]. Am J Epidemiol, 2013, 177(11): 1 255-1 262.
[11] JOHNSON J D, GIBSON S J, OBER R E. Cholestyramine-enhanced fecal elimination of carbon-14 in rats after administration of ammonium[14C]Perfluorooctanoate or Potassium [14C]Perfluorooctanesulfonate [J]. Toxicological Sciences, 1984, 4(6): 972-976.
[12] ZOU W, LIU W, YANG B, et al. Quercetin protects against perfluorooctanoic acid-induced liver injury by attenuating oxidative stress and inflammatory response in mice [J]. International Immunopharmacology, 2015, 28(1): 129-135.
[13] LIU W, XU C, SUN X, et al. Grape seed proanthocyanidin extract protects against perfluorooctanoic acid-induced hepatotoxicity by attenuating inflammatory response, oxidative stress and apoptosis in mice [J]. Toxicology Research, 2016, 5(1): 224-234.
[14] 翟齐啸. 乳酸菌减除镉危害的作用及机制研究[D].无锡:江南大学,2015.
[15] 刘云才,张娟,焦聪聪,等. 乳酸菌对铜暴露大鼠肝功能及氧化应激的影响[J].青岛大学医学院学报, 2017, 53(2):198-202.
[16] 韩佳萦,苏伊玲,熊丽,等. 塑化剂DEHP暴露对小鼠巨噬细胞的免疫毒性作用[J].农业环境科学学报, 2018, 37(4):673-679.
[17] 李秋月,许海玉,杨洪军.促炎因TNF-α,IL-1β,IL-6在神经病理性疼痛中的研究进展[J].中国中药杂志, 2017,42(19):3 709-3 712.
[18] 邢家溧.植物乳杆菌缓解典型全氟及多氟烷基化合物毒性及机制研究[D]. 无锡:江南大学,2017.
[19] MOLLENHAUER M A M, BRADSHAW S G, FAIR P A, et al. Effects of perfluorooctane sulfonate (PFOS) exposure on markers of inflammation in female B6C3F1 mice[J]. Journal of environmental science and health. Part A, 2011, 46(2): 97-108.
[20] 郑丽,董光辉,潘艳艳,等.全氟辛烷磺酸对雄性小鼠免疫状态的影响[J]. 环境与健康杂志, 2011,28(3):189-191.
[21] MIR H, MEENA A S, CHAUDHRY K K, et al. Occludin deficiency promotes ethanol-induced disruption of colonic epithelial junctions, gut barrier dysfunction and liver damage in mice[J]. BBA - General Subjects, 2016, 1 860(4): 765-774.
[22] 马姝丽,李小芹,王菊平.酪酸梭菌对胆汁淤积大鼠的肠黏膜通透性和紧密连接蛋白的影响[J]. 实用医学杂志, 2018, 34(6):69-72.
[23] 徐万里,陆高,梁世杰,等.短链脂肪酸介导的菌群-宿主互动与肠易激综合征的研究进展[J]. 世界华人消化杂志,2015,23(36):5 815-5 822.
[24] REILLY R J, ROMBEAU J L. Metabolism and potential clinical application of short chain fatty acid[J]. Clinical Nutrition, 1993, 12(Suppl 1):97-105.
[25] BULTMAN S J. Molecular pathways: Gene-environment interactions regulating dietary fiber induction of proliferation and apoptosis via butyrate for cancer prevention[J]. Clinical Cancer Research, 2014, 20 (4):799-803.
[26] FUKUDA S, TOH H, HASE K, et al. Bifidobacteria can protect from enteropathogenic infection through production of acetate[J]. Nature, 2012, 469 (7 331):543-547.