Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>

6-PPD quinone (6-PPDQ) is a derivative from 6-PPD, an antioxidant added in tires. Leucine is an important amino acid that needs to be obtained from the diet. In <i>Caenorhabditis elegans</i>, we examined the effect of 6-PPDQ exposure at environmentally relevant concentrations (ERCs) on t...

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Main Authors: Wei Wang, Yunhui Li, Dayong Wang
Format: Article
Language:English
Published: MDPI AG 2025-06-01
Series:Toxics
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Online Access:https://www.mdpi.com/2305-6304/13/7/544
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author Wei Wang
Yunhui Li
Dayong Wang
author_facet Wei Wang
Yunhui Li
Dayong Wang
author_sort Wei Wang
collection DOAJ
description 6-PPD quinone (6-PPDQ) is a derivative from 6-PPD, an antioxidant added in tires. Leucine is an important amino acid that needs to be obtained from the diet. In <i>Caenorhabditis elegans</i>, we examined the effect of 6-PPDQ exposure at environmentally relevant concentrations (ERCs) on the content of leucine and underlying mechanisms. In nematodes, 0.1–10 μg/L of 6-PPDQ decreased leucine content. The expression of the <i>aat-1</i>-encoding amino acid transmembrane transporter was decreased by 0.1–10 μg/L of 6-PPDQ, and leucine content was reduced by <i>aat-1</i> RNAi. Meanwhile, the expression of <i>bcat-1</i>-encoding branched-chain amino acid transferase was increased by 0.1–10 μg/L of 6-PPDQ, and leucine content was increased by <i>bcat-1</i> RNAi. Additionally, the expressions of <i>dbt-1</i> and <i>ivd-1</i> encoding two enzyme genes governing NADH and FADH<sub>2</sub> generations were decreased by 0.1–10 μg/L of 6-PPDQ, and their expressions in 6-PPDQ exposed nematodes were increased by <i>bcat-1</i> RNAi. After 6-PPDQ exposure, NADH content was reduced by <i>dbt-1</i> RNAi, and FADH<sub>2</sub> content was reduced by <i>ivd-1</i> RNAi. Moreover, 6-PPDQ-induced mitochondrial dysfunction and other aspects of toxicity (such as intestinal ROS generation and lipofuscin accumulation, inhibited locomotion, and reduced brood size) were suppressed by <i>bcat-1</i> RNAi and strengthened by <i>dbt-1</i> and <i>ivd-1</i> RNAi. The 6-PPDQ-induced toxicity and the decrease in <i>dbt-1</i> and <i>ivd-1</i> expressions could be inhibited by following leucine (5 mM) treatment. Our results demonstrate the important association of leucine adsorption and catabolism with 6-PPDQ toxicity induction.
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spelling doaj-art-874a5afd85d94e1381028f3565bb7c542025-08-20T03:32:35ZengMDPI AGToxics2305-63042025-06-0113754410.3390/toxics13070544Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>Wei Wang0Yunhui Li1Dayong Wang2Shenzhen Ruipuxun Academy for Stem Cell & Regenerative Medicine, Shenzhen 518122, ChinaSchool of Public Health, Southeast University, Nanjing 210009, ChinaShenzhen Ruipuxun Academy for Stem Cell & Regenerative Medicine, Shenzhen 518122, China6-PPD quinone (6-PPDQ) is a derivative from 6-PPD, an antioxidant added in tires. Leucine is an important amino acid that needs to be obtained from the diet. In <i>Caenorhabditis elegans</i>, we examined the effect of 6-PPDQ exposure at environmentally relevant concentrations (ERCs) on the content of leucine and underlying mechanisms. In nematodes, 0.1–10 μg/L of 6-PPDQ decreased leucine content. The expression of the <i>aat-1</i>-encoding amino acid transmembrane transporter was decreased by 0.1–10 μg/L of 6-PPDQ, and leucine content was reduced by <i>aat-1</i> RNAi. Meanwhile, the expression of <i>bcat-1</i>-encoding branched-chain amino acid transferase was increased by 0.1–10 μg/L of 6-PPDQ, and leucine content was increased by <i>bcat-1</i> RNAi. Additionally, the expressions of <i>dbt-1</i> and <i>ivd-1</i> encoding two enzyme genes governing NADH and FADH<sub>2</sub> generations were decreased by 0.1–10 μg/L of 6-PPDQ, and their expressions in 6-PPDQ exposed nematodes were increased by <i>bcat-1</i> RNAi. After 6-PPDQ exposure, NADH content was reduced by <i>dbt-1</i> RNAi, and FADH<sub>2</sub> content was reduced by <i>ivd-1</i> RNAi. Moreover, 6-PPDQ-induced mitochondrial dysfunction and other aspects of toxicity (such as intestinal ROS generation and lipofuscin accumulation, inhibited locomotion, and reduced brood size) were suppressed by <i>bcat-1</i> RNAi and strengthened by <i>dbt-1</i> and <i>ivd-1</i> RNAi. The 6-PPDQ-induced toxicity and the decrease in <i>dbt-1</i> and <i>ivd-1</i> expressions could be inhibited by following leucine (5 mM) treatment. Our results demonstrate the important association of leucine adsorption and catabolism with 6-PPDQ toxicity induction.https://www.mdpi.com/2305-6304/13/7/544leucineadsorptioncatabolismmitochondrial functionpharmacological treatmentnematodes
spellingShingle Wei Wang
Yunhui Li
Dayong Wang
Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
Toxics
leucine
adsorption
catabolism
mitochondrial function
pharmacological treatment
nematodes
title Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
title_full Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
title_fullStr Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
title_full_unstemmed Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
title_short Exposure to 6-PPD Quinone Disrupts Adsorption and Catabolism of Leucine and Causes Mitochondrial Dysfunction in <i>Caenorhabditis elegans</i>
title_sort exposure to 6 ppd quinone disrupts adsorption and catabolism of leucine and causes mitochondrial dysfunction in i caenorhabditis elegans i
topic leucine
adsorption
catabolism
mitochondrial function
pharmacological treatment
nematodes
url https://www.mdpi.com/2305-6304/13/7/544
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