Acetyl- l -carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats

Bodaghi-Namileh, Vida; Sepand, Mohammad Reza; Omidi, Abdollah; Aghsami, Mehdi; Seyednejad, Seyed Afshin; Kasirzadeh, Sara; Sabzevari, Omid

doi:10.1016/j.etap.2017.12.005

Cited by 62 publications

(28 citation statements)

References 39 publications

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“…The anti-inflammatory activity of L-carnitine could be attributed to the attenuation of NF-KB, the principal activator of most pro-inflammatory cytokines as TNF-α and interleukins. This explanation coincides with the recent findings of BODAGHI-NAMILEH et al (2018) who mentioned that co-administration of carnitine with arsenic, down-regulated NF-KB expression, suggesting the anti-inflammatory activity of carnitine and suppression of oxidative stress. Recently, L-carnitine supplementation was found to diminish interleukins levels in aspartame induced toxicity in rats (HAMZA et al, 2019).…”

Section: Discussionsupporting

confidence: 92%

L-carnitine mitigates bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats

et al. 2020

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bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats. Vet. arhiv 90, 57-68, 2020. AbSTrACT Bisphenol, used in many polycarbonate plastics and epoxy resins industries, exerts toxic effects on mammalian organs. The mechanisms underlying bisphenol toxicity are well understood, however the chemoprevention effects of L-carnitine have not yet been recorded. This study aimed to explore the protective mechanism of L-carnitine against BPA-induced hepatotoxicity. Male rats were randomly distributed into 4 groups of 10 rats each: vehicle (5 mL corn oil/kg), bisphenol (50 mg/kg b.w. orally), L-carnitine (500 mg/kg b.w. i/p), and L-carnitine bisphenol pre-treated groups. Bisphenol was dissolved in corn oil and gavaged for 70 consecutive days. Up-regulation of tumor necrosis factor (6.6-fold), and interleukin 6 (3.2-fold) mRNA transcript, along with suppression of nuclear factor erythroid 2-like 2 (0.4-fold), were recorded, following bisphenol administration. Subsequently, bisphenol provoked oxidative stress and attenuated the antioxidative molecules. Finally, hepatic dysfunction was assessed by elevated serum aminotransferases, alkaline phosphatase, lactate dehydrogenase, glutamyl transferase activities and ammonia levels, with the subsequent decline in serum albumin concentration, which confirmed the inflammatory cell infiltration and hydropic degeneration, and the impairment of lipid profile. Interestingly, co-administration of L-carnitine improved liver function and lipid profile, which was explained by the activation of nuclear factor erythroid 2-like 2 (1.5-fold) mRNA transcript, which augmented the antioxidant levels and suppressed oxidative stress, tumor necrosis factor (2.6fold), and interleukin 6 (1.5-fold) gene expression. In conclusion, L-carnitine exerted hepatoprotective activity against bisphenol toxicity via antioxidant and anti-inflammatory effects.

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Section: Discussionsupporting

confidence: 92%

L-carnitine mitigates bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats

et al. 2020

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“…A recent study on mice showed similar results after 6 weeks of arsenic treatment in male mice. Hepatic arsenic level was increased up to 15-20 folds in dose group (Podder et al, 2014;Bodaghi-Namileh et al, 2018;Tasnim et al, 2015) showed similar results after administration of arsenic doses of 20, 50 and 100 mg/kg BW. Arsenic produces reactive nitrogen species (RNS) and reactive oxygen species (ROS).…”

Section: Discussionsupporting

confidence: 56%

Genetic and Morphological Characterization of Lebanese Mountain Local Goat Population

2020

THE JAPS

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Inorganic arsenic is a well-known toxicant and carcinogen. Millions of people in world are being affected by arsenic mainly through drinking water. Objectives: To evaluate toxic effects of sodium arsenate (Na3 AsO4) and assess protective role of garlic (Allium sativum) in minimizing its toxicological effects. Methodology: In this study, 20 pregnant female mice were divided into 4 groups. Group I (Control) was healthy control and Group II (Dose group) was orally administered with 50mg/kg of Na3 AsO4 on the "Gestation day 6" for consecutive 6 days. Group III (Dose+ Antidote group) mice were administered with 50mg/kg of Na3 AsO4 and garlic extract (30mg/kg) with a gap of one hour. Group IV (Antidote Group) was administered orally with garlic extract (30mg/kg). Results: Pregnant female mice were sacrificed at 18 th day of gestation, Na3 AsO4 affected weight, limbs, and size of the fetus. It also caused pyknosis, necrosis and increased sinusoidal space, fibrosis in both mother and fetal liver of mice. High mortality rate and pregnancies loss were observed in Group II. On the other hand, garlic showed strong antioxidant activity which neutralized oxidative stress condition in both mother and fetal liver of mice in Group III. Conclusion: Our findings indicated that Na3 AsO4 is a potential toxic metalloid that can cross placenta and garlic is equally effective in ameliorating these toxicities in mice.

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“…Duan et al found that acute arsenic exposure induced NF-κB activation and then stimulated the generation of inflammatory factors to induce the development of inflammation in the spleen and thymus of mice [ 7 ]. Arsenic could induce inflammation, which also was occurred in humans [ 14 ], rats [ 30 ], dendritic cells [ 18 , 31 ] and avian brain tissue [ 32 ], etc. As shown in our study, we found that the spleen continuous NF-κB of arsenic-exposed mice, that was, it did not change with the extension of the exposure time (even for 12 months).…”

Section: Discussionmentioning

confidence: 99%

Chronic arsenic exposure induces the time-dependent modulation of inflammation and immunosuppression in spleen

Yan

Zhang

et al. 2020

Cell Biosci

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Background Arsenic exposure has become a matter of worldwide concern, which is associated with immune-related diseases. However, little is known about its effect on inflammatory immune-related homeostasis. The purpose of our study was to understand the potential tuning of above responses exerted by chronic arsenic exposure. Methods Kunming mice were treated with 25 and 50 mg/L sodium arsenite for 1, 3 and 12 months via drinking water. At different endpoints of arsenic exposure, all animals and the whole spleen of the mice were weighed. The total arsenic levels of spleen were determined by the HPLC-HG-AFS method. Splenic NF-κB, MAPK and NRF2 protein levels by treatment of 25 mg/L NaAsO 2 for 1, 3 and 12 months and 25 mg/L and 50 mg/L NaAsO 2 for 12 months were assessed by western blot. Total RNA of spleen was isolated and relative mRNA levels of Foxp3 , Il - 10 , Tnf - α , Il - 6 , Ifn - γ , Il - 1β and Il - 12 were measured by real-time PCR. Results Our results shown that NF-κB were continuously activated with treatment of 25 mg/L arsenic from 1, 3 to 12 months and 50 mg/L arsenic for 12 months. The transcription factor Foxp3 increased at 1 month but decreased at 3 and 12 months no matter 25 or 50 mg/L arsenic exposure. However, cytokine Il - 10 always showed increased trend in mice treated with 25 or 50 mg/L arsenic for 1, 3 and 12 months. The transcriptional profiles of Tnf - α , Il - 1β , Il - 6 , Ifn - γ and Il - 12 revealed transient elevation at 1 and 3 months but shown significant decrease at 12 months on the whole. In addition, the sustained activation of inflammatory MAPK and anti-oxidative Nrf2 signaling pathways were observed in mice exposed to arsenic for 1, 3 and 12 months. Conclusion In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-κB as well as the increased transcription level of Foxp3 and Il - 10 .

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Acetyl- l -carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats

Cited by 62 publications

References 39 publications

L-carnitine mitigates bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats

L-carnitine mitigates bisphenol A-induced hepatic toxicity via activation of Nrf2 and inhibition of pro-inflammatory cytokine gene expression in rats

Genetic and Morphological Characterization of Lebanese Mountain Local Goat Population

Chronic arsenic exposure induces the time-dependent modulation of inflammation and immunosuppression in spleen

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