Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats

Aim: Long-term exposure to excess sodium fluoride (NaF) can cause chronic fluorosis. Liver, the most important detoxification organ, is the most vulnerable to the effects of fluoride. Sodium butyrate (NaB), a short-chain fatty acid produced in the intestinal tract, maintains normal mitochondrial fun...

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Main Authors: Jing Xia, Xiaolin Zhang, Leiyu Xu, Nan Yan, Zhenxiang Sun, Xiaoxu Duan, Lu Meng, Rong Qi, Fu Ren, Zhengdong Wang
Format: Article
Language:English
Published: Elsevier 2025-02-01
Series:Ecotoxicology and Environmental Safety
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Online Access:http://www.sciencedirect.com/science/article/pii/S0147651325001575
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author Jing Xia
Xiaolin Zhang
Leiyu Xu
Nan Yan
Zhenxiang Sun
Xiaoxu Duan
Lu Meng
Rong Qi
Fu Ren
Zhengdong Wang
author_facet Jing Xia
Xiaolin Zhang
Leiyu Xu
Nan Yan
Zhenxiang Sun
Xiaoxu Duan
Lu Meng
Rong Qi
Fu Ren
Zhengdong Wang
author_sort Jing Xia
collection DOAJ
description Aim: Long-term exposure to excess sodium fluoride (NaF) can cause chronic fluorosis. Liver, the most important detoxification organ, is the most vulnerable to the effects of fluoride. Sodium butyrate (NaB), a short-chain fatty acid produced in the intestinal tract, maintains normal mitochondrial function in vivo and reduces liver inflammation and oxidative stress. This study aims to investigate the protective effect and potential mechanism of NaB on liver injury in fluoride poisoned rats, particularly through the mitophagy pathway. Methods: Rats were randomly divided into four groups of 12 male rats each: control, NaF (100 mg/mL), NaB (1000 mg/kg), and NaF (100 mg/mL)+NaB (1000 mg/kg) group. Key findings: Changes in the levels of liver enzymes (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], and malondialdehyde [MDA]) confirmed NaF-induced liver injury. NaF also changed the levels of autophagy markers (Beclin-1, LC3α/β, P62), and increased the level of apoptosis. The combined use of NaB and NaF significantly ameliorated these indices. Significance: These findings indicate that NaB may provide effective protection against NaF-induced liver injury through its attenuates oxidative stress, apoptosis, and excessive mitophagy mechanisms.
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spelling doaj-art-d6ca93ad9b5e47d0b84120c209e4c4de2025-01-31T05:10:01ZengElsevierEcotoxicology and Environmental Safety0147-65132025-02-01291117821Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in ratsJing Xia0Xiaolin Zhang1Leiyu Xu2Nan Yan3Zhenxiang Sun4Xiaoxu Duan5Lu Meng6Rong Qi7Fu Ren8Zhengdong Wang9Liaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR ChinaDepartment of General Surgery, Central Hospital Affiliated to Shenyang Medical College, Shengyang, PR ChinaLiaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR ChinaRehabilitation Medical Scool, Shenyang Medical College, Shengyang, PR ChinaLiaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR ChinaSchool of Public Health College, Shenyang Medical College, Shenyang, PR ChinaLiaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR ChinaLaboratory of Molecular Morphology, Basic Medical College, Shenyang Medical College, Shengyang, PR ChinaLiaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR China; Corresponding authors.Liaoning Province Key Laboratory for phenomics of Human Ethnic Specificity and Critical Illness, Shenyang Medical College, Shengyang, PR China; Corresponding authors.Aim: Long-term exposure to excess sodium fluoride (NaF) can cause chronic fluorosis. Liver, the most important detoxification organ, is the most vulnerable to the effects of fluoride. Sodium butyrate (NaB), a short-chain fatty acid produced in the intestinal tract, maintains normal mitochondrial function in vivo and reduces liver inflammation and oxidative stress. This study aims to investigate the protective effect and potential mechanism of NaB on liver injury in fluoride poisoned rats, particularly through the mitophagy pathway. Methods: Rats were randomly divided into four groups of 12 male rats each: control, NaF (100 mg/mL), NaB (1000 mg/kg), and NaF (100 mg/mL)+NaB (1000 mg/kg) group. Key findings: Changes in the levels of liver enzymes (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], and malondialdehyde [MDA]) confirmed NaF-induced liver injury. NaF also changed the levels of autophagy markers (Beclin-1, LC3α/β, P62), and increased the level of apoptosis. The combined use of NaB and NaF significantly ameliorated these indices. Significance: These findings indicate that NaB may provide effective protection against NaF-induced liver injury through its attenuates oxidative stress, apoptosis, and excessive mitophagy mechanisms.http://www.sciencedirect.com/science/article/pii/S0147651325001575FluorosisLiverMitophagySodium butyrateSodium fluoride
spellingShingle Jing Xia
Xiaolin Zhang
Leiyu Xu
Nan Yan
Zhenxiang Sun
Xiaoxu Duan
Lu Meng
Rong Qi
Fu Ren
Zhengdong Wang
Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
Ecotoxicology and Environmental Safety
Fluorosis
Liver
Mitophagy
Sodium butyrate
Sodium fluoride
title Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
title_full Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
title_fullStr Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
title_full_unstemmed Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
title_short Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats
title_sort sodium butyrate attenuates oxidative stress apoptosis and excessive mitophagy in sodium fluoride induced hepatotoxicity in rats
topic Fluorosis
Liver
Mitophagy
Sodium butyrate
Sodium fluoride
url http://www.sciencedirect.com/science/article/pii/S0147651325001575
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