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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Elsevier
2025-02-01
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| 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. |
| format | Article |
| id | doaj-art-d6ca93ad9b5e47d0b84120c209e4c4de |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| 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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