Plasma and red cell lipids in alcoholics with macrocytosis

Clemens, Michael; Kessler, Winfried; Schied, H. W.; Schupmann, A.; Waller, H. D.

doi:10.1016/0009-8981(86)90075-6

Cited by 27 publications

(9 citation statements)

References 18 publications

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“…These findings are consistent with the observation that alcoholics have more plasma E18:1 as a percent of total FAEE than do binge drinkers (25). Alcoholics also tend to increase their fatty acid composition in plasma and cell membranes in general toward oleate (38)(39)(40).…”

Section: Resultssupporting

confidence: 88%

Red blood cell fatty acid ethyl esters: a significant component of fatty acid ethyl esters in the blood

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Cluette‐Brown

Teruya

et al. 2003

Journal of Lipid Research

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An association between alcoholism and abnormal red blood cell (RBC) size and shape has long been recognized (1). However, the underlying pathophysiologic mechanisms responsible for the morphologic alterations are incompletely understood (2-6). Fatty acid ethyl esters (FAEEs), esterification products of ethanol and fatty acids, have been shown to be incorporated into phospholipid bilayers up to 30 mol % of total membrane fatty acids (7). FAEEs have been implicated as mediators of ethanolinduced organ damage (8-13) and have clinical utility as markers for ethanol intake (14, 15). Serum and plasma FAEE levels closely correlate with blood ethanol levels, but these circulating FAEEs in blood persist for at least 24 h after ethanol ingestion, long after ethanol is no longer detectable (15, 16).Although the largest reservoir of FAEE synthetic capability appears to reside in the pancreas and the liver (17, 18), enzyme activity that catalyzes FAEE synthesis has been detected in RBCs, white blood cells (WBCs), and platelets. Given the much higher concentration of RBCs in the blood, it has been suggested that RBCs may provide a significant portion of the total FAEE synthase activity in whole blood (19). With this information, the possibility that RBC membranes might synthesize and sequester FAEEs in the blood has been raised.We conducted a controlled clinical trial to determine if FAEEs accumulate and persist within RBCs following ethanol ingestion. The objectives of this study were to determine: 1 ) whether FAEEs appear in RBCs following ethanol ingestion and whether RBC-associated FAEEs correlate with blood ethanol concentration; 2 ) how long FAEEs persist in RBCs after ethanol intake is discontinued; 3 ) whether the fatty acid composition of RBC FAEEs is distinct from the fatty acid composition of FAEEs in plasma; and 4 ) whether RBC and plasma FAEE species undergo a remodeling process with changes in fatty acid composition following discontinuation of ethanol ingestion. METHODSThe study was approved by the institutional review board of the Massachusetts General Hospital. A written informed consent was obtained from each volunteer prior to subject enrollment.Abbreviations: AIC, akaike information criteria; E16:0, ethyl palmitate; E18:0, ethyl stearate; E18:1, ethyl oleate; E18:2, ethyl linoleate; FAEE, fatty acid ethyl ester; GC-MS, gas liquid chromatography-mass spectrometry; RBC, red blood cell; SPE, solid-phase extraction; WBC, white blood cell.

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Section: Resultssupporting

confidence: 88%

Red blood cell fatty acid ethyl esters: a significant component of fatty acid ethyl esters in the blood

Best

Cluette‐Brown

Teruya

et al. 2003

Journal of Lipid Research

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“…Significance values (*P<0.05) were determined vs. baseline associated depletion of RBC ATP may damage the antioxidant defence system and induce some RBC membrane changes such as oxidative damage, promoting extravascular haemolysis via the reticuloendothelial system. Up to this time, changes of the membrane lipid composition have been reported as one of the reducing factors of the membrane fluidity; an increase in C/PL ratio [16,17] and a decrease in PC/SM ratio [18]. Especially, some investigators reported that the reduction in fluidity of RBCs was a consequence of the altered RBC membrane lipid composition and was due to an increased membrane C/PL ratio [19,20].…”

Section: Discussionmentioning

confidence: 96%

Changes in serum and red blood cell membrane lipids in patients treated with interferon ribavirin for chronic hepatitis C

et al. 2005

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One of the side effects by interferon ribavirin (I/R) treatment is haemolytic anemia, causing some patients to discontinue I/R treatment. The exact mechanism of I/R-induced anemia is unknown. The aim of this study is to evaluate the effects of I/R treatment on the serum lipid and red blood cell (RBC) membrane lipid profiles of patients with chronic hepatitis C (CHC) and the association between changes of RBC membrane lipids and haemolytic anemia by I/R treatment. Fourteen patients with CHC were treated with I/R and their serum lipid profiles were studied. In addition, in seven of the 14 patients, the RBC membrane lipid profiles were analysed. In the RBC membrane lipid composition, the total cholesterol, total phospholipids and cholesterol/phospholipids (C/PL) ratio were significantly increased. Phosphatidylcholine (PC) and the phosphatidylcholine/ sphingomyelin (PC/SM) ratio were significantly decreased and other phospholipid fractions were significantly increased. Changes in the serum lipids and RBC membrane lipid profiles of patients with CHC treated with I/R were shown. Especially, a decrease in the RBC deformability and membrane fluidity by changes in these RBC membrane lipids was supposed and it is suggested that those changes may result in haemolytic anemia by I/R treatment.

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“…Evidence shows that alcohol‐induced changes can cause a significant decrease in arachidonic acid in human plasma, erythrocytes, platelets and liver tissue (38–40). Arachidonic acid is released from phospholipids inserted into the plasma membrane by the action of Ca 2+ ‐dependent phospholipase 2 (PLA 2 ) (41).…”

Section: Effects On Iron‐induced Hepatic Toxicity In Ratsmentioning

confidence: 99%

Pharmacological actions of curcumin in liver diseases or damage

Rivera-Espinoza

Muriel

2009

Liver International

156

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Since 1900 BC, several therapeutic activities have been attributed to the rhizomes of the plant Curcuma longa for a variety of diseases, including liver disorders. Curcumin, the main active compound obtained from this plant, was first isolated two centuries ago and its structure as diferuloylmethane was determined in 1910. Curcumin has shown anti-inflammatory, anti-oxidant, antifungal, antibacterial and anticancer activities. The pharmacological properties of curcumin were reviewed recently and focused mainly on its anticancer properties. However, its beneficial activity on liver diseases (known centuries ago, and demonstrated recently utilizing animal models) has not being reviewed in depth until now. The curcumin ability to inhibit several factors like nuclear factor-kB, which modulates several pro-inflammatory and profibrotic cytokines as well as its anti-oxidant properties, provide a rational molecular basis to use it in hepatic disorders. Curcumin attenuates liver injury induced by ethanol, thioacetamide, iron overdose, cholestasis and acute, subchronic and chronic carbon tetrachloride (CCl 4 ) intoxication; moreover, it reverses CCl 4 cirrhosis to some extent. Unfortunately, the number of studies of curcumin on liver diseases is still very low and investigations in this area must be encouraged because hepatic disorders constitute one of the main causes of worldwide mortality.

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Plasma and red cell lipids in alcoholics with macrocytosis

Cited by 27 publications

References 18 publications

Red blood cell fatty acid ethyl esters: a significant component of fatty acid ethyl esters in the blood

Red blood cell fatty acid ethyl esters: a significant component of fatty acid ethyl esters in the blood

Changes in serum and red blood cell membrane lipids in patients treated with interferon ribavirin for chronic hepatitis C

Pharmacological actions of curcumin in liver diseases or damage

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