Interaction of cartinine with mitochondrial cardiolipin

Battelli, Daniele; Bellei, Monica; Arrigoni-Martelli, E; Muscatello, Umberto; Bobyleva, Valentina

doi:10.1016/0304-4165(92)90158-q

Cited by 31 publications

(16 citation statements)

References 24 publications

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“…These findings are in line with the current literature where we and other groups could demonstrate protective effects of L -carnitine on ultrastructural levels in various models [29,47,50,51,52]. …”

Section: Discussionsupporting

confidence: 93%

L-Carnitine Ameliorates L-Asparaginase-Induced Acute Liver Toxicity in Steatotic Rat Livers

et al. 2013

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Background: Chemotherapy with L-asparaginase is associated with hepatotoxicity resulting in organ dysfunction in patients with preexisting liver disorders. This study investigated the protective effect of L-carnitine during chemotherapy in a steatotic rat liver model. Methods: Livers from nonsteatotic and steatotic rats were tested in an isolated liver reperfusion model adding L-asparaginase and L-carnitine to the reperfusate. Portal venous pressure (PVP), hepatic oxygen consumption, aspartate aminotransferase, lactate dehydrogenase, glutamate dehydrogenase and α-glutathione S-transferase levels were assessed. Further histopathological analysis was performed and cytotoxicity was verified in vitro. Results:L-Asparaginase induced toxicity in fatty livers whereas low toxicity was observed in normal livers. L-Carnitine induced a decline in PVP and oxygen consumption, and reduced parenchymal and mitochondrial damage in fatty livers. Cytotoxicity of L-asparaginase was not impaired by the presence of L-carnitine. Conclusions: Our study emphasizes the potential of L-carnitine to reduce L-asparaginase-induced hepatotoxicity in patients with preexisting liver disorders.

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Section: Discussionsupporting

confidence: 93%

L-Carnitine Ameliorates L-Asparaginase-Induced Acute Liver Toxicity in Steatotic Rat Livers

et al. 2013

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“…This effect could be due to stabilization of hepatocyte membranes by L-carnitine with the consequent decrease in the leakage of liver enzymes. Indeed, the interaction of L-carnitine with sarcolemmal phospholipids and mitochondrial membranes has been previously reported [49] . In carnitine-depleted rats, DENA produced a progressive increase in the activities of liver enzymes as well as massive degenerative changes and evidence of pre-neoplastic lesions in liver tissues ( Figure 2C).…”

Section: Discussionmentioning

confidence: 92%

Progression of diethylnitrosamine-induced hepatic carcinogenesis in carnitine-depleted rats

Al-Rejaie¹,

Aleisa²,

Al-Yahya³

et al. 2009

WJG

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AIM:To investigate whether carnitine deficiency is a risk factor during the development of diethylnitrosamine (DENA)-induced hepatic carcinogenesis. METHODS:A total of 60 male Wistar albino rats were divided into six groups with 10 animals in each group. Rats in group 1 (control group) received a single intraperitoneal (i.p.) injection of normal saline. Animals in group 2 (carnitine-supplemented group) were given L-carnitine (200 mg/kg per day) in drinking water for 8 wk. Animals in group 3 (carnitine-depleted group) were given D-carnitine (200 mg/kg per day) and mildronate (200 mg/kg per day) in drinking water for 8 wk. Rats in group 4 (DENA group) were injected with a single dose of DENA (200 mg/kg, i.p.) and 2 wk later received a single dose of carbon tetrachloride (2 mL/kg) by gavage as 1:1 dilution in corn oil. Animals in group 5 (DENA-carnitine depleted group) received the same treatment as group 3 and group 4. Rats in group 6 (DENA-carnitine supplemented group) received the same treatment as group 2 and group 4. RESULTS:Administration of DENA resulted in a significant increase in alanine transaminase (ALT), g a m m a -g l u t a my l t ra n s fe ra s e ( G -G T ) , a l k a l i n e phosphatase (ALP), total bilirubin, thiobarbituric acid reactive substances (TBARS) and total nitrate/ nitrite (NOx) and a significant decrease in reduced glutathione (GSH), glutathione peroxidase (GSHPx), catalase (CAT) and total carnitine content in liver tissues. In the carnitine-depleted rat model, DENA induced a dramatic increase in serum ALT, G-GT, ALP and total bilirubin, as well as a progressive reduction in total carnitine content in liver tissues. Interestingly, L-carnitine supplementation resulted in a complete reversal of the increase in liver enzymes, TBARS and NOx, and a decrease in total carnitine, GSH, GSHPx, and CAT induced by DENA, compared with the control values. Histopathological examination of liver tissues confirmed the biochemical data, where L-carnitine prevented DENA-induced hepatic carcinogenesis while D-carnitine-mildronate aggravated DENA-induced hepatic damage. CONCLUSION:Data from this study suggest for the first time that: (1) carnitine deficiency is a risk factor and should be viewed as a mechanism in DENAinduced hepatic carcinogenesis; (2) oxidative stress plays an important role but is not the only cause of DENA-induced hepatic carcinogenesis; and (3) long-term L-carnitine supplementation prevents the development of DENA-induced liver cancer.

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“…Alterations in membrane lipid composition, such as decreases in cardiolipin content or changes in the ω-3/ω-6 ratio, impair the electron transport chain and energy production (29), ion channel and Ca 2+ homeostasis of the mitochondria and of the cell (30)(31)(32)(33). These alterations can also impair carnitine-mediated lipid transport, mitochondrial lipid metabolism (34,35), cholesterol biosynthesis (36)(37)(38)(39), activity of the pyruvate dehydrogenase complex (40,41) and, finally, cause activation of the apoptosis pathway (42). In the present study, detailed electron microscopy of human RPE cells from aged and AMD specimens are described.…”

Section: Introductionmentioning

confidence: 99%

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

Bianchi

Scarinci

Ripandelli

et al. 2012

International Journal of Molecular Medicine

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Abstract. Age-related macular degeneration (AMD) is the leading cause of impaired vision and blindness in the aging population. The aims of our studies were to identify qualitative and quantitative alterations in mitochondria in human retinal pigment epithelium (RPE) from AMD patients and controls and to test the protective effects of pigment epithelium-derived factor (PEDF), a known neurotrophic and antiangiogenic substance, against neurotrophic keratouveitis. Histopathological alterations were studied by means of morphometry, light and electron microscopy. Unexpectedly, morphometric data showed that the RPE alterations noted in AMD may also develop in normal aging, 10-15 years later than appearing in AMD patients. Reduced tear secretion, corneal ulceration and leukocytic infiltration were found in capsaicin (CAP)-treated rats, but this effect was significantly attenuated by PEDF. These findings suggest that PEDF accelerated the recovery of tear secretion and also prevented neurotrophic keratouveitis and vitreoretinal inflammation. PEDF may have a clinical application in inflammatory and neovascular diseases of the eye.

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Interaction of cartinine with mitochondrial cardiolipin

Cited by 31 publications

References 24 publications

L-Carnitine Ameliorates L-Asparaginase-Induced Acute Liver Toxicity in Steatotic Rat Livers

L-Carnitine Ameliorates L-Asparaginase-Induced Acute Liver Toxicity in Steatotic Rat Livers

Progression of diethylnitrosamine-induced hepatic carcinogenesis in carnitine-depleted rats

Retinal pigment epithelium, age-related macular degeneration and neurotrophic keratouveitis

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