Determination of free and total carnitine in plasma by an enzymatic reaction and spectrophotometric quantitation spectrophotometric determination of carnitine

Prieto, José Manuel Compaña; Andrade, Fernando; Aldámiz‐Echevarría, Luis; Sanjurjo, Pablo

doi:10.1016/j.clinbiochem.2006.06.005

Cited by 35 publications

(16 citation statements)

References 30 publications

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“…The serum level of L-carnitine and total L-carnitine was done following a Prieto et al method 42. Detection of IL-6, TNF-α, IGF-1, and vitamin D in the serum was done using enzyme-linked immunosorbent assay kits (R&D Systems, Inc., Minneapolis, MN, USA) and assessed using spectrophotometry.…”

Section: Methodsmentioning

confidence: 99%

Efficacy of L-carnitine supplementation on frailty status and its biomarkers, nutritional status, and physical and cognitive function among prefrail older adults: a double-blind, randomized, placebo-controlled clinical trial

Badrasawi

Shahar

Zahara

et al. 2016

CIA

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BackgroundFrailty is a biological syndrome of decreased reserve and resistance to stressors due to decline in multiple physiological systems. Amino acid deficiency, including L-carnitine, has been proposed to be associated with its pathophysiology. Nevertheless, the efficacy of L-carnitine supplementation on frailty status has not been documented. Thus, this study aimed to determine the effect of 10-week L-carnitine supplement (1.5 g/day) on frailty status and its biomarkers and also physical function, cognition, and nutritional status among prefrail older adults in Klang Valley, Malaysia.MethodologyThis study is a randomized, double-blind, placebo-controlled clinical trial conducted among 50 prefrail subjects randomized into two groups (26 in L-carnitine group and 24 in placebo group). Outcome measures include frailty status using Fried criteria and Frailty Index accumulation of deficit, selected frailty biomarkers (interleukin-6, tumor necrosis factor-alpha, and insulin-like growth factor-1), physical function, cognitive function, nutritional status and biochemical profile.ResultsThe results indicated that the mean scores of Frailty Index score and hand grip test were significantly improved in subjects supplemented with L-carnitine (P<0.05 for both parameters) as compared to no change in the placebo group. Based on Fried criteria, four subjects (three from the L-carnitine group and one from the control group) transited from prefrail status to robust after the intervention.ConclusionL-carnitine supplementation has a favorable effect on the functional status and fatigue in prefrail older adults.

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Section: Methodsmentioning

confidence: 99%

Efficacy of L-carnitine supplementation on frailty status and its biomarkers, nutritional status, and physical and cognitive function among prefrail older adults: a double-blind, randomized, placebo-controlled clinical trial

Badrasawi

Shahar

Zahara

et al. 2016

CIA

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“…Total carnitine concentrations were determined in serum, urine and cardiac tissues according to the method reported by Prieto et al59 In brief, carnitine reacts with acetyl-CoA forming acetylcarnitine in areaction mediated by carnitine acetyltransferase enzyme. The liberated CoA-SH reacts with 5,5-dithiobis-(2-nitrobenzoic acid) and forming thiophenolate ion, whose generation is proportional to the amount of carnitine and can be measured spectrophotometrically at 412 nm.…”

Section: Methodsmentioning

confidence: 99%

Carnitine Deficiency and Oxidative Stress Provoke Cardiotoxicity in an Ifosfamide‐Induced Fanconi Syndrome Rat Model

Sayed‐Ahmed

Darweesh

Fatani

2010

Oxidative Medicine and Cellular Longevity

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In addition to hemorrhagic cystitis, Fanconi Syndrome is a serious clinical side effect during ifosfamide (IFO) therapy. Fanconi syndrome is a generalized dysfunction of the proximal tubule which is characterized by excessive urinary excretion of glucose, phosphate, bicarbonate, amino acids and other solutes excreted by this segment of the nephron including L-carnitine. Carnitine is essential cofactor for β-oxidation of long-chain fatty acids in the myocardium. IFO therapy is associated with increased urinary carnitine excretion with subsequent secondary deficiency of the molecule. Cardiac abnormalities in IFO-treated cancer patients were reported as isolated clinical cases. This study examined whether carnitine deficiency and oxidative stress, secondary to Fanconi Syndrome, provoke IFO-induced cardiomyopathy as well as exploring if carnitine supplementation using Propionyl-L-carnitine (PLC) could offer protection against this toxicity. In the current study, an animal model of carnitine deficiency was developed in rats by D-carnitine-mildronate treatment Adult male Wistar albino rats were assigned to one of six treatment groups: the first three groups were injected intraperitoneally with normal saline, D-carnitine (DC, 250 mg/kg/day) combined with mildronate (MD, 200 mg/kg/day) and PLC (250 mg/kg/day), respectively, for 10 successive days. The 4th, 5th and 6th groups were injected with the same doses of normal saline, DC-MD and PLC, respectively for 5 successive days before and 5 days concomitant with IFO (50 mg/kg/day). IFO significantly increased serum creatinine, blood urea nitrogen (BUN), urinary carnitine excretion and clearance, creatine phosphokinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), intramitochondrial acetyl-CoA/CoA-SH and thiobarbituric acid reactive substances (TBARS) in cardiac tissues and significantly decreased adenosine triphosphate (ATP) and total carnitine and reduced glutathione (GSH) content in cardiac tissues. In carnitine-depleted rats, IFO induced dramatic increase in serum creatinine, BUN, CK-MB, LDH, carnitine clearance and intramitochondrial acetyl-CoA/CoA-SH, as well as progressive reduction in total carnitine and ATP in cardiac tissues. Interestingly, PLC supplementation completely reversed the biochemical changes-induced by IFO to the control values. In conclusion, data from the present study suggest that: Carnitine deficiency and oxidative stress, secondary to Fanconi Syndrome, constitute risk factors and should be viewed as mechanisms during development of IFO-induced cardiotoxicity. Carnitine supplementation, using PLC, prevents the development of IFO-induced cardiotoxicity through antioxidant signalling and improving mitochondrial function.

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“…Total carnitine concentration was determined in kidney tissues according to the method reported by Prieto et al [28]. In brief, carnitine reacts with acetyl-CoA, forming acetylcarnitine in a reaction mediated by carnitine acetyltransferase enzyme.…”

Section: Determination Of Total Carnitine In Rat Kidney Tissuesmentioning

confidence: 99%

Progression of cyclophosphamide-induced acute renal metabolic damage in carnitine-depleted rat model

Sayed‐Ahmed

2010

Clin Exp Nephrol

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Determination of free and total carnitine in plasma by an enzymatic reaction and spectrophotometric quantitation spectrophotometric determination of carnitine

Cited by 35 publications

References 30 publications

Efficacy of L-carnitine supplementation on frailty status and its biomarkers, nutritional status, and physical and cognitive function among prefrail older adults: a double-blind, randomized, placebo-controlled clinical trial

Efficacy of L-carnitine supplementation on frailty status and its biomarkers, nutritional status, and physical and cognitive function among prefrail older adults: a double-blind, randomized, placebo-controlled clinical trial

Carnitine Deficiency and Oxidative Stress Provoke Cardiotoxicity in an Ifosfamide‐Induced Fanconi Syndrome Rat Model

Progression of cyclophosphamide-induced acute renal metabolic damage in carnitine-depleted rat model

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