Oral S-adenosylmethionine in the symptomatic treatment of intrahepatic cholestasis

Frezza, M; Surrenti, C.; Manzillo, G; Fiaccadori, F; Bortolini, M.; Padova, C. Di

doi:10.1016/0016-5085(90)91250-a

Cited by 157 publications

(70 citation statements)

References 26 publications

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“…SAMe administration just before APAP treatment greatly diminished the extent of centrilobular necrosis in C57BL/6 male mice compared with animals given APAP (Valentovic et al, 2004). SAMe has also shown beneficial effects in reducing and reversing hepatic damage induced by alcohol in humans (Lieber, 2002) and in intrahepatic cholestasis (Frezza et al, 1990).…”

Section: Acetaminophen (Apap) or N-(4-hydroxyphenyl Acetamide)mentioning

confidence: 96%

Comparison of S-Adenosyl-l-methionine and N-Acetylcysteine Protective Effects on Acetaminophen Hepatic Toxicity

Terneus

Kiningham²,

Carpenter³

et al. 2006

J Pharmacol Exp Ther

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Nutraceuticals are widely used by the general public, but very little information is available regarding the effects of nutritional agents on drug toxicity. Excessive doses of acetaminophen (APAP, 4-hydroxyacetanilide) induce hepatic centrilobular necrosis. The naturally occurring substance S-adenosyl-L-methionine (SAMe) has been reported to reduce the hepatic toxicity of APAP. The present study was designed to investigate the hepatoprotective effects of SAMe in comparison to the clinically used antidote N-acetylcysteine (NAC). Male C57BL/6 mice were injected intraperitoneally (i.p.) with an equimolar dose (1.25 mmol/kg) of either SAMe or NAC just before APAP, and the groups were denoted SAMeϩAPAP and NACϩAPAP, respectively. Mice were immediately injected i.p. with 300 mg/kg APAP, and hepatotoxicity was evaluated after 4 h. SAMe was more hepatoprotective than NAC at a dose of 1.25 mmol/kg as liver weight was unchanged by APAP injection in the SAMeϩAPAP group, whereas liver weight was increased in the NACϩAPAP group. SAMe was more hepatoprotective for APAP toxicity than NAC, because alanine aminotransferase levels were lower in the SAMeϩAPAP. Pretreatment with SAMe maintained total hepatic glutathione (GSH) levels higher than NAC pretreatment before APAP, although total hepatic GSH levels were lower in the SAMeϩAPAP and NACϩAPAP groups than the vehicle control values. Oxidative stress was less extensive in the SAMeϩAPAP group compared with the APAPtreated mice as indicated by Western blots for protein carbonyls and 4-hydroxynonenal-adducted proteins. In summary, SAMe reduced APAP toxicity and was more potent than NAC in reducing APAP hepatotoxicity.

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Section: Acetaminophen (Apap) or N-(4-hydroxyphenyl Acetamide)mentioning

confidence: 96%

Comparison of S-Adenosyl-l-methionine and N-Acetylcysteine Protective Effects on Acetaminophen Hepatic Toxicity

Terneus

Kiningham²,

Carpenter³

et al. 2006

J Pharmacol Exp Ther

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“…113 Patients with intrahepatic cholestasis were also administered SAMe, and improvements in their serum transaminases and bilirubin have been reported by several workers. [113][114][115] A pivotal study from Mato's group reported that SAMe supplementation improved mortality and decreased need for liver transplantation in patients with less severe alcoholic cirrhosis. 116 This was a multicenter trial from Spain enrolling 123 patients.…”

Section: Therapeutic Trialsmentioning

confidence: 98%

The Use of Selected Nutrition Supplements and Complementary and Alternative Medicine in Liver Disease

et al. 2006

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“…SAM has also been used to treat various types of acute and chronic liver diseases. Although the focus of clinical trials in this area has been diffuse, a number of clinical trials have focused on the effect of SAM on cholestasis arising from a variety of causes, including pregnancy [66][67][68]. SAM may exert beneficial effects on the liver through a variety of mechanisms.…”

Section: Sam and The Blood Brain Barriermentioning

confidence: 99%

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Cavallaro¹,

Fuso²,

D’Erme³

et al. 2016

Int J Clin Nutr Diet

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S-adenosyl-L-methionine (SAM) is the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. SAM level in the organism decreases with aging and restoring the original levels through exogenous supplementation is an important tool for the improvement of many vital functions. Indeed, SAM deficiency may contribute to the onset of several diseases, i.e. depression, liver diseases, osteoarthritis and senile neurological disorders such as Alzheimer's and Parkinson's diseases. Recent evidences indicate that SAM may have an involvement in oxidative stress, a process which typically involves an alteration of cellular sulfur amino acids homeostasis. SAM is not only the principal methyl donor, but also a precursor of glutathione, the major endogenous antioxidant, whose role in counteracting oxidative stress is well known. In this review we will highlight the role of SAM not just as a methyl-donor but also as a regulator of different metabolic pathways involved in the antioxidant response in brain related disorders. Role of S-adenosylmethionine in the Modulation of Oxidative StressRelated Neurodegeneration Review ArticleOpen Access IntroductionThe interaction between environmental and genetic factors plays a fundamental role in inducing and modulating the aging processes towards brain disorders. Among environmental factors, diet and nutritional lifestyle have a key role in brain health through the alteration of the intake or the bioavailability of metabolites and cofactors. Specific nutritional factors have particular impact on one-carbon metabolism, which is a complex biochemical pathway regulated by the presence of folate, vitamin B12 and B6 (among other metabolites) and leading to the production of S-adenosyl-L-methionine (SAM), the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. This metabolism involves three interrelated biochemical pathways: folate cycle, transsulfuration pathway and methionine cycle. These three metabolic sequences were first combined and correlated in 1964 by Laster's group [1][2][3] giving the integrated point of view of transmethylation and transsulfuration pathways, linking sulfur amino acid metabolism to the provision of methyl groups for many biochemical processes. Normal functioning of this metabolic cycle is essential for growth and development and impairment of this metabolism; transmethylation efficiency is associated with many diseases like cardiovascular diseases [4][5], liver diseases [6-9], neural tube defects [10] and brain diseases [11][12][13][14][15][16]. One-carbon metabolism alterations, low methylation and oxidative stress are all linked to Late Onset Alzheimer's Disease (LOAD) [17][18][19][20][21][22][23][24] Moreover, wide confirmed reports underline the role of SAM dependent reactions in age related neurodegeneration also showi...

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Oral S-adenosylmethionine in the symptomatic treatment of intrahepatic cholestasis

Cited by 157 publications

References 26 publications

Comparison of S-Adenosyl-l-methionine and N-Acetylcysteine Protective Effects on Acetaminophen Hepatic Toxicity

Comparison of S-Adenosyl-l-methionine and N-Acetylcysteine Protective Effects on Acetaminophen Hepatic Toxicity

The Use of Selected Nutrition Supplements and Complementary and Alternative Medicine in Liver Disease

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

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