Effects of L-carnitine supplementation on biomarkers of oxidative stress, antioxidant capacity and lipid profile, in patients with pemphigus vulgaris: a randomized, double-blind, placebo-controlled trial

Mohammadi, Hamed; Djalali, Mahmoud; Daneshpazhooh, Maryam; Honarvar, Niaz Mohammadzadeh; Chams‐Davatchi, Cheyda; Sepandar, Farnaz; Fakhri, Zahra; Yaghubi, Elham; Zarei, Mahnaz; Javanbakht, Mohammad Hassan

doi:10.1038/ejcn.2017.131

Cited by 21 publications

(13 citation statements)

References 36 publications

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“…This result was in agreement with MALAGUARNERA et al (2010), who found that L-carnitine ameliorated the blood glucose, TAG, cholesterol, and lipoprotein concentrations in NASH patients. Also, pemphigus valugaris patients had low levels of serum total cholesterol, TAG, and LDL-c without any change in HDL-c level, following L-carnitine administration (MOHAMMADI et al, 2018). The reduction in the serum LDL-c concentration may be attributed to the enhancement of LDL receptor expression by L-carnitine (YOUSEFINEJAD et al, 2015).…”

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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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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“…The meta-analysis of the studies enrolling haemodialysis patients suggests that L-carnitine supplementation may positively affect serum LDL level, although it was not associated with a significant change in serum TCh, HDL and TG levels [49]. Similarly, lipid profile improves following L-carnitine supplementation in patients with pemphigus vulgaris [50] and in women with knee osteoarthritis [51]. In the present study, significant reduction in serum TCh, LDL and TG concentrations has been observed following 24-weeks supplementation, but not attributable to L-carnitine.…”

Section: Discussion/conclusionmentioning

confidence: 99%

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

et al. 2018

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Background: L-carnitine can be metabolized to trimethylamine N-oxide (TMAO), a molecule that promotes atherogenesis through its interaction with macrophages and lipid metabolism. Objective: The aim of the present study was to assess whether L-carnitine supplementation may promote changes in selected serum biomarkers of atherosclerosis. Methods: Before the start, in the mid-point and after completing the 24-weeks supplementation protocol, fasting blood samples were taken from the antecubital vein. Plasma free L-carnitine and TMAO were determined by the UPLC/MS/MS method. Serum proteins were determined by the enzyme immunoassay method using commercially available kits. Total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides have been determined using standard automatic analyzer. Results: L-carnitine supplementation elevated fasting plasma carnitine in the mid-point of our study and it remained increased until the end of supplementation period. Moreover, it induced tenfold increase in plasma TMAO concentration but did not affect serum C-reactive protein, interleukin-6, tumour necrosis factor-α, L-selectin, P-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 or lipid profile markers. Conclusion: We demonstrated that although oral L-carnitine supplementation significantly increased plasma TMAO concentration, no lipid profile changes or other markers of adverse cardiovascular events were detected in healthy aged women over the period of 24 weeks.

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“…To have more detailed view, mitochondria, peroxisomes, various types of oxidases, ascorbic acid oxidation and cytochrome as well as ultraviolet/ionizing radiations, chemotherapeutics, stress, and environmental toxins can be named as sources of production of endogenous ROS [63] . Protective antioxidants enzymes can effectively decompose ROS at their mild states however; the condition can change to toxic levels if the production rate surpasses much more than the antioxidant system capacity [64] , [65] . As an example, endogenous and exogenous ROS could affect lens crystallins as of a biological target.…”

Section: Oxidative Stress Conceptmentioning

confidence: 99%

Review on oxidative stress relation on COVID-19: Biomolecular and bioanalytical approach

Ebrahimi

Norouzi

Aazami

et al. 2021

International Journal of Biological Macromolecules

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Effects of L-carnitine supplementation on biomarkers of oxidative stress, antioxidant capacity and lipid profile, in patients with pemphigus vulgaris: a randomized, double-blind, placebo-controlled trial

Cited by 21 publications

References 36 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

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

Review on oxidative stress relation on COVID-19: Biomolecular and bioanalytical approach

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