Ameliorative effects of l-carnitine on rats raised on a diet supplemented with lead acetate

El-Sherbini, El-Said; El-Sayed, Ghada M.; Shotory, Rehab El; Gheith, Nervana; Abou-Alsoud, Mohamed; Harakeh, Steve; Karrouf, Gamal

doi:10.1016/j.sjbs.2016.08.010

Cited by 23 publications

(14 citation statements)

References 63 publications

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“…In line with an increasing number of evidence, our results showed LC ability to reduce ROS production and contemporarily to rise the expression of antioxidant enzymes, i.e. SOD, catalase and phospholipid hydroperoxide glutathione peroxidase in an in vitro, in vivo models and humans [41][42][43][44]. In this regard, our group established this LC ability in skeletal muscle cells model, cardiomyocytes and osteoblastic cells observing that this anti-oxidant action is strictly correlated with calcium signaling [18-20, 26, 41].…”

Section: Representative Immunoblots Are Shownsupporting

confidence: 87%

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Montesano

Senesi

Vacante

et al. 2019

J Endocrinol Invest

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Purpose Nonalcoholic fatty liver disease (NAFLD) is defined by excessive lipid accumulation in the liver and involves an ample spectrum of liver diseases, ranging from simple uncomplicated steatosis to cirrhosis and hepatocellular carcinoma. Accumulating evidence demonstrates that high fructose intake enhances NAFLD development and progression promoting inhibition of mitochondrial β-oxidation of long-chain fatty acids and oxidative damages. l-Carnitine (LC), involved in β-oxidation, has been used to reduce obesity caused by high-fat diet, which is beneficial to ameliorating fatty liver diseases. Moreover, in the recent years, various studies have established LC anti-oxidative proprieties. The objective of this study was to elucidate primarily the underlying anti-oxidative mechanisms of LC in an in vitro model of fructose-induced liver steatosis. Methods Human hepatoma HepG2 cells were maintained in medium supplemented with LC (5 mM LC) with or without 5 mM fructose (F) for 48 h and 72 h. In control cells, LC or F was not added to medium. Fat deposition, anti-oxidative, and mitochondrial homeostasis were investigated. Results LC supplementation decreased the intracellular lipid deposition enhancing AMPK activation. However, compound C (AMPK inhibitor-10 μM), significantly abolished LC benefits in F condition. Moreover, LC, increasing PGC1 α expression, ameliorates mitochondrial damage-F induced. Above all, LC reduced ROS production and simultaneously increased protein content of antioxidant factors, SOD2 and Nrf2. Conclusion Our data seemed to show that LC attenuate fructose-mediated lipid accumulation through AMPK activation. Moreover, LC counteracts mitochondrial damages and reactive oxygen species production restoring antioxidant cellular machine. These findings provide new insights into LC role as an AMPK activator and anti-oxidative molecule in NAFLD.

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Section: Representative Immunoblots Are Shownsupporting

confidence: 87%

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Montesano

Senesi

Vacante

et al. 2019

J Endocrinol Invest

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“…We found that mean SOD enzyme expression in control group (K+) was lower than that in control group (K-). This finding was in line with the previous research that the administration of lead acetate in a dose of 24 mg/kg bw/day per sonde for one month resulted in lower blood erythrocyte SOD enzyme levels compared to control group that received water, 16 also stated that exposure to lead acetate of 100 mg/kg bw mixed with corn oil in rats decreased hepatic SOD enzymes compared to that of control group. 17 Other researchers also reported that white rats injected with lead acetate of 20 mg/kg bw for 11 days had lower mean testicular SOD enzymes than control group.…”

Section: Discussionsupporting

confidence: 92%

Nanocurcumin Potential Effect of SOD Enzyme and Caspase-3 Expression in Lead-Acetate Induced Rats Ovarian Granulosa Cells

Syarifah¹,

Sudjarwo²,

Hendarto³

et al. 2021

Indian Journal of Forensic Medicine & Toxicology

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Aim: This study investigated the potential effect of nanocurcumin on the increase of SOD enzyme expression and decrease of caspase-3 in lead acetate-induced rats ovarian granulosa cells.Materials and Methods: Forty five female rats were divided into 5 groups, the negative control group (rats receiving corn oil, one hour later receiving distilled water), positive control group (rats receiving corn oil, one hour later receiving lead acetate of 40 mg/kg bw) and experimental groups 1, 2 and 3 (rats receiving nanocurcumin 50 mg, 100 mg and 200 mg/kg bw). One hour after administering the nanocurcumin, the rats received 40 mg/kg of lead acetate. All groups received oral treatment once a day for 26 days. On day 27 the rats were sacrificed and the expression of SOD and caspase-3 enzymes were measured using immunohistochemical methods.Results: This study found that lead acetate decreased SOD enzyme expression and increased caspase-3. In contrast, nanocurcumin increased SOD enzyme and decreased caspase-3 expression in lead acetate-induced rats ovarian granulosa cells. Conclusion:Nanocurcumin has potential as a strong natural antioxidant by affecting the increase of SOD and the decrease of caspase-3 cells in lead acetate-induced rats ovarian granulosa cells.

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“…Recently, L-carnitine supplementation was found to diminish interleukins levels in aspartame induced toxicity in rats (HAMZA et al, 2019). In the same context, EL-SHERBINI et al (2017) attributed the protective role of L-carnitine against lead toxicity to ROS production attenuation and free radical scavenging activities via augmentation of antioxidant enzymes. Also, FATEN et al (2013) suggested the protective activity of L-carnitine against methotrexate-induced oxidative insult via improvement of hepatic GSH levels, and enzymatic antioxidant activities.…”

Section: Discussionmentioning

confidence: 99%

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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Ameliorative effects of l-carnitine on rats raised on a diet supplemented with lead acetate

Cited by 23 publications

References 63 publications

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Nanocurcumin Potential Effect of SOD Enzyme and Caspase-3 Expression in Lead-Acetate Induced Rats Ovarian Granulosa Cells

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

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