PMID- 35476938
OWN - NLM
STAT- MEDLINE
DCOM- 20220524
LR  - 20220524
IS  - 1873-6351 (Electronic)
IS  - 0278-6915 (Linking)
VI  - 164
DP  - 2022 Jun
TI  - Endogenous hydrogen sulfide counteracts polystyrene nanoplastics-induced 
      mitochondrial apoptosis and excessive autophagy via regulating Nrf2 and PGC-1alpha 
      signaling pathway in mouse spermatocyte-derived GC-2spd(ts) cells.
PG  - 113071
LID - S0278-6915(22)00269-1 [pii]
LID - 10.1016/j.fct.2022.113071 [doi]
AB  - Nanoplastics (NaPs) has reported to accumulate in the testes and cause 
      degeneration in the seminiferous tubules. Additionally, exogenous hydrogen 
      sulfide (H(2)S) is proposed to enhance tolerance to oxidative stress. The current 
      work aimed to investigate the mechanisms of NaPs-induced reproductive toxicity in 
      vitro and probable reproductive protection by endogenous H(2)S. We firstly found 
      that 80 nm fluorescent NaPs could enter into GC-2spd(ts) cells by fluorescent 
      inverted microscope. In addition, we demonstrated that NaPs-induced could induce 
      ROS-dependent mitochondrial apoptosis and autophagy in vitro. Our results showed 
      that the H(2)S donor NaHS ameliorated NaPs-triggered mitochondrial apoptosis and 
      autophagy in GC-2spd(ts) cells. Moreover, NaPs treatment did not change the 
      interaction between nuclear factor erythroid-derived 2-related factor (Nrf2) and 
      Kelch-like ECH associated protein 1 (Keap1), while inhibiting nuclear 
      accumulation of Nrf2 protein was observed. Meanwhile, NaHS weakened this 
      interaction, subsequently improving antioxidant ability via increasing the 
      protein levels of heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 
      (NQO1). Further, invitro experiments showed that NaPs-induced reproductive 
      toxicity associated with reducing PGC-1alpha. Meanwhile, NaPs-induced higher 
      expression PGC-1alpha was further enhanced by NaHS co-treatment. Together, this study 
      highlight that exogenous H(2)S should be an essential therapeutic approach to 
      alleviate NaPs-induced reproductive toxicity via regulating Nrf2/PGC-1alpha signal.
CI  - Copyright (c) 2022 Elsevier Ltd. All rights reserved.
FAU - Li, Siwen
AU  - Li S
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China. Electronic address: lisiwen0529@163.com.
FAU - Ma, Yu
AU  - Ma Y
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China.
FAU - Ye, Shuzi
AU  - Ye S
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China.
FAU - Su, Ying
AU  - Su Y
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China.
FAU - Hu, Die
AU  - Hu D
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China.
FAU - Xiao, Fang
AU  - Xiao F
AD  - Xiangya School of Public Health, Central South University, Changsha, 410078, PR 
      China. Electronic address: fangxiao@csu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20220426
PL  - England
TA  - Food Chem Toxicol
JT  - Food and chemical toxicology : an international journal published for the British 
      Industrial Biological Research Association
JID - 8207483
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (Microplastics)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Polystyrenes)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Autophagy
MH  - *Hydrogen Sulfide/metabolism/pharmacology
MH  - Kelch-Like ECH-Associated Protein 1/metabolism
MH  - Male
MH  - Mice
MH  - Microplastics
MH  - *NF-E2-Related Factor 2/genetics/metabolism
MH  - Oxidative Stress
MH  - Polystyrenes
MH  - Signal Transduction
MH  - Spermatocytes
OTO - NOTNLM
OT  - Mitochondrial apoptosis
OT  - Nanoplastics
OT  - Nuclear factor erythroid-derived 2-related factor (Nrf2)
OT  - Pyruvate kinase M2
OT  - Reproductive toxicity
EDAT- 2022/04/28 06:00
MHDA- 2022/05/25 06:00
CRDT- 2022/04/27 20:02
PHST- 2022/03/29 00:00 [received]
PHST- 2022/04/17 00:00 [revised]
PHST- 2022/04/20 00:00 [accepted]
PHST- 2022/04/28 06:00 [pubmed]
PHST- 2022/05/25 06:00 [medline]
PHST- 2022/04/27 20:02 [entrez]
AID - S0278-6915(22)00269-1 [pii]
AID - 10.1016/j.fct.2022.113071 [doi]
PST - ppublish
SO  - Food Chem Toxicol. 2022 Jun;164:113071. doi: 10.1016/j.fct.2022.113071. Epub 2022 
      Apr 26.