PMID- 38513858
OWN - NLM
STAT- MEDLINE
DCOM- 20240417
LR  - 20240426
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 926
DP  - 2024 May 20
TI  - Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused 
      oxidative stress to activate NF-kappaB/NLRP3 pathway aggravated pyroptosis and 
      inflammation in mouse kidney.
PG  - 171817
LID - S0048-9697(24)01960-0 [pii]
LID - 10.1016/j.scitotenv.2024.171817 [doi]
AB  - Polystyrene microplastic (PS-MPs) contamination has become a worldwide hotspot of 
      concern, and its entry into organisms can cause oxidative stress resulting in 
      multi-organ damage. The plasticizer di (2-ethylhexyl) phthalate (DEHP) is a 
      common endocrine disruptor, these two environmental toxins often occur together, 
      but their combined toxicity to the kidney and its mechanism of toxicity are 
      unknown. Therefore, in this study, we established PS-MPS and/or DEHP-exposed 
      mouse models. The results showed that alone exposure to both PS-MPs and DEHP 
      caused inflammatory cell infiltration, cell membrane rupture, and content 
      spillage in kidney tissues. There were also down-regulation of antioxidant enzyme 
      levels, increased ROS content, activated of the NF-kappaB pathway, stimulated the 
      levels of heat shock proteins (HSPs), pyroptosis, and inflammatory associated 
      factors. Notably, the co-exposure group showed greater toxicity to kidney 
      tissues, the cellular assay further validated these results. The introduction of 
      the antioxidant n-acetylcysteine (NAC) and the NLRP3 inhibitor (MCC950) could 
      mitigate the changes in the above measures. In summary, co-exposure of PS-MPs and 
      DEHP induced oxidative stress that activated the NF-kappaB/NLRP3 pathway and 
      aggravated kidney pyroptosis and inflammation, as well as that HSPs are also 
      involved in this pathologic injury process. This study not only enriched the 
      nephrotoxicity of plasticizers and microplastics, but also provided new insights 
      into the toxicity mechanisms of multicomponent co-pollution in environmental.
CI  - Copyright (c) 2024 Elsevier B.V. All rights reserved.
FAU - Li, Shanshan
AU  - Li S
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, 
      PR China.
FAU - Gu, Xuedie
AU  - Gu X
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, 
      PR China.
FAU - Zhang, Muyue
AU  - Zhang M
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, 
      PR China.
FAU - Jiang, Qihang
AU  - Jiang Q
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, 
      PR China.
FAU - Xu, Tong
AU  - Xu T
AD  - College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, 
      PR China.. Electronic address: tongxu@neau.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20240319
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
RN  - 0 (Antioxidants)
RN  - C42K0PH13C (Diethylhexyl Phthalate)
RN  - 0 (Microplastics)
RN  - 0 (NF-kappa B)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 6O7F7IX66E (phthalic acid)
RN  - 0 (Phthalic Acids)
RN  - 0 (Plasticizers)
RN  - 0 (Plastics)
RN  - 0 (Polystyrenes)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Antioxidants/metabolism
MH  - *Diethylhexyl Phthalate/toxicity/metabolism
MH  - Inflammation/chemically induced
MH  - Kidney/metabolism
MH  - *Microplastics/metabolism/toxicity
MH  - NF-kappa B/metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - *Oxidative Stress
MH  - *Phthalic Acids
MH  - Plasticizers/toxicity/metabolism
MH  - Plastics/metabolism/toxicity
MH  - Polystyrenes/toxicity/metabolism
MH  - *Pyroptosis
OTO - NOTNLM
OT  - Di (2-ethylhexyl) phthalate
OT  - Inflammation
OT  - Kidney toxicity
OT  - Polystyrene microplastics
OT  - Pyroptosis
OT  - ROS
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2024/03/22 00:44
MHDA- 2024/04/17 06:42
CRDT- 2024/03/21 20:27
PHST- 2024/01/08 00:00 [received]
PHST- 2024/03/15 00:00 [revised]
PHST- 2024/03/17 00:00 [accepted]
PHST- 2024/04/17 06:42 [medline]
PHST- 2024/03/22 00:44 [pubmed]
PHST- 2024/03/21 20:27 [entrez]
AID - S0048-9697(24)01960-0 [pii]
AID - 10.1016/j.scitotenv.2024.171817 [doi]
PST - ppublish
SO  - Sci Total Environ. 2024 May 20;926:171817. doi: 10.1016/j.scitotenv.2024.171817. 
      Epub 2024 Mar 19.