| S-Adenosyl methionine |
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IUPAC name
(2S)-2-Amino-4-[[(2S,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methyl-methylsulfonio]butanoate
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Other names
S-Adenosyl-L-methionine; ademetionine; SAM-e; SAMe
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| Identifiers |
| CAS number |
29908-03-0 Y |
| PubChem |
9865604 |
| ChemSpider |
8041295 Y |
| MeSH |
S-Adenosylmethionine |
| ChEMBL |
CHEMBL24991 N |
| ATC code |
A16AA02 |
| Jmol-3D images |
Image 1 |
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O=C(O)C(N)CC[S+](C)C[C@H]3O[C@@H](n2cnc1c(ncnc12)N)[C@H](O)[C@@H]3O
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InChI=1S/C15H22N6O5S/c1-27(3-2-7(16)15(24)25)4-8-10(22)11(23)14(26-8)21-6-20-9-12(17)18-5-19-13(9)21/h5-8,10-11,14,22-23H,2-4,16H2,1H3,(H2-,17,18,19,24,25)/p+1/t7?,8-,10-,11-,14-,27?/m1/s1 Y
Key: MEFKEPWMEQBLKI-YDBXVIPQSA-O Y
InChI=1/C15H22N6O5S/c1-27(3-2-7(16)15(24)25)4-8-10(22)11(23)14(26-8)21-6-20-9-12(17)18-5-19-13(9)21/h5-8,10-11,14,22-23H,2-4,16H2,1H3,(H2-,17,18,19,24,25)/p+1/t7?,8-,10-,11-,14-,27?/m1/s1
Key: MEFKEPWMEQBLKI-NNGIMXIKBF
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| Properties |
| Molecular formula |
C15H22N6O5S+ |
| Molar mass |
398.44 g/mol |
N (verify) (what is: Y/N?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
| Infobox references |
S-Adenosyl methionine (ademetionine, SAM, SAMe, SAM-e) is a common cosubstrate involved in methyl group transfers. SAM was first discovered in Italy by G. L. Cantoni in 1952.[1] It is made from adenosine triphosphate (ATP) and methionine by methionine adenosyltransferase (EC 2.5.1.6). Transmethylation, transsulfuration, and aminopropylation are the metabolic pathways that use SAM. Although these anabolic reactions occur throughout the body, most SAM is produced and consumed in the liver.[1]
The methyl group (CH3) attached to the methionine sulfur atom in SAM is chemically reactive. This allows donation of this group to an acceptor substrate in transmethylation reactions. More than 40 metabolic reactions involve the transfer of a methyl group from SAM to various substrates, such as nucleic acids, proteins, lipids and secondary metabolites.
In bacteria, SAM is bound by the SAM riboswitch, which regulates genes involved in methionine or cysteine biosynthesis.
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Contents
- 1 Biochemistry of S-adenosyl methionine
- 1.1 SAM cycle
- 1.2 Radical SAM enzymes
- 1.3 Polyamine biosynthesis
- 2 Therapeutic uses
- 3 Oral forms, usage and adverse effects
- 3.1 Oral forms
- 3.2 Usage
- 3.3 Adverse effects
- 3.4 Possible side effects
- 3.5 Interactions and contraindications
- 4 See also
- 5 References
- 6 External links
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Biochemistry of S-adenosyl methionine
SAM cycle
The reactions that produce, consume, and regenerate SAM are called the SAM cycle. In the first step of this cycle, the SAM-dependent methylases (EC 2.1.1) that use SAM as a substrate produce S-adenosyl homocysteine as a product.[2] This is hydrolysed to homocysteine and adenosine by S-adenosylhomocysteine hydrolase EC 3.3.1.1 and the homocysteine recycled back to methionine through transfer of a methyl group from 5-methyltetrahydrofolate, by one of the two classes of methionine synthases (i.e. cobalamin-dependent (EC 2.1.1.13) or cobalamin-independent (EC 2.1.1.14)). This methionine can then be converted back to SAM, completing the cycle.[3]
Radical SAM enzymes
A large number of iron-sulfur cluster-containing enzymes cleave SAM reductively to produce a 5′-deoxyadenosyl 5′-radical as an intermediate, and are called radical SAM enzymes.[4] Most enzymes with this capability share a region of sequence homology that includes the motif CxxxCxxC or a close variant. The radical intermediate allows enzymes to perform a wide variety of unusual chemical reactions. Examples of radical SAM enzymes include spore photoproduct lyase, activases of pyruvate formate lyase and anaerobic sulfatases, lysine 2,3-aminomutase, and various enzymes of cofactor biosynthesis, peptide modification, metalloprotein cluster formation, tRNA modification, lipid metabolism, etc. Some radical SAM enzymes use a second SAM as a methyl donor. Radical SAM enzymes are much more abundant in anaerobic bacteria than in aerobic organisms.
Polyamine biosynthesis
Another major role of SAM is in polyamine biosynthesis. Here, SAM is decarboxylated by adenosylmethionine decarboxylase (EC 4.1.1.50) to form S-adenosylmethioninamine. This compound then donates its n-propylamine group in the biosynthesis of polyamines such as spermidine and spermine from putrescine.[5]
SAM is required for cellular growth and repair. It is also involved in the biosynthesis of several hormones and neurotransmitters that affect mood, such as dopamine and serotonin. Methyltransferases are also responsible for the addition of methyl groups to the 2' hydroxyls of the first and second nucleotides next to the 5' cap in messenger RNA.[6][7]
Therapeutic uses
In the United States and Canada, SAM is sold as a nutritional supplement under the marketing name SAM-e (also spelled SAME or SAMe; pronounced "sam ee" or "Sammy"). SAM is also marketed under the Gumbaral, Samyr, Adomet, Heptral and Admethionine brand names as a prescription drug approved in Russia, Italy, and Germany. Some research, including multiple clinical trials, has indicated taking SAM on a regular basis may help fight depression,[8][9][10] liver disease, and the pain of osteoarthritis.[11] All other indications are not yet proven.
Therapeutic use of SAM has increased in the US, as dietary supplements have gained in popularity, especially after the Dietary Supplement Health and Education Act was passed in 1994. This law allowed the distribution of SAM as a dietary supplement, and therefore allowed it to bypass the regulatory requirements for drugs of the Food and Drug Administration (FDA).
At first, a line of evidence suggested abnormally low levels of endogenous SAM may play an important role in the development of Alzheimer's disease (AD), and that SAM may therefore have therapeutic potential in the treatment of AD. However, further research has indicated this effect is likely due to vitamin B12 deficiencies, which result in neurologic defects due to the inability to conduct one carbon transfers (with folate) in the absence of B12. Severely low levels of SAM have been found in the cerebrospinal fluid[12] and in all brain regions of AD patients examined.[13] Preliminary research suggests SAM may have therapeutic potential in treating AD patients[14] and a recent study using a mouse model of AD found that supplementary SAM prevented oxidative damage and cognitive impairment.[15]
SAMe is a methyl donor and is involved in the synthesis of various neurotransmitters in the brain. Derived from the amino acid L-methionine through a metabolic pathway called the one-carbon cycle, SAMe has been postulated to have antidepressant properties. [16] SAMe may enhance the impact of mood-boosting messengers such as serotonin and dopamine—either by regulating their breakdown or by speeding production of the receptor molecules they latch on to. There is evidence that SAMe helps fight depression. Since the 1970s, there have been 40 clinical studies involving roughly 1400 patients and the results have been remarkably consistent. In 1994, Dr. Giorgio Bressa, a psychiatrist at the University Cattolica Sacro Cuore in Rome found that, “The efficacy of SAMe in treating depressive syndromes…is superior to that of a placebo and comparable to that of standard…antidepressants. [17]
SAMe has been studied in the treatment of osteoarthritis. SAMe reduces the pain associated with osteoarthritis. Although an optimal dose has yet to be determined, SAMe appears as effective as the non-steroidal anti-inflammatory drugs. Additional study is warranted to confirm these findings. [18]
Oral forms, usage and adverse effects
Oral forms
Oral SAM achieves peak plasma concentrations three to five hours after ingestion of an enteric-coated tablet (400–1000 mg). The half-life is about 100 minutes.[19] It may require up to one month for it to reach full effectiveness in treating osteoarthritis.[19] Because of structural instability, stable salt forms of SAM are required for its use as an oral drug. The University of Maryland lists the commonly used salts: tosylate, butanedisulfonate, disulfate tosylate, disulfate ditosylate, and disulfate monotosylate.[20]
With the advent of FDA-mandated good manufacturing practices (GMPs) in 2008, manufacturers are required to confirm their products contain what is listed on the label through the end of shelf life. Whether they achieve this goal or not has been questioned. This testing has shown that properly produced and packaged SAM has a shelf life in excess of three years; however, most manufacturers label for a two-year shelf life.
Claims that the SAM butanedisulfonate salt is more stable or better absorbed are not supported by the references usually cited as evidence. Different salts have successfully been used in clinical trials, but there is no published head-to-head comparison.[20][21][22]
Usage
SAM is best absorbed on an empty stomach.[23] Enteric-coated tablets packaged in foil or foil blister packs increase stability and improve absorption. SAM should be stored in a cool, dry place to prevent deterioration.[20]
Adverse effects
Gastrointestinal disorder, dyspepsia and anxiety can occur with SAM consumption.[19] Long-term effects are unknown. SAM is a weak DNA-alkylating agent.[24]
Possible side effects
Once SAM donates its methyl group to choline, in the formation of creatine, carnitine, DNA, tRNA, norepinephrine, and other compounds, it is transformed into S-adenosyl-homocysteine, (SAH). Under normal circumstances, homocysteine, in the presence of vitamin B6, vitamin B12, and folic acid (SAM's main cofactors), will eventually be converted back into methionine, SAM, or cysteine, glutathione, and other useful substances. However, if adequate amounts of these vitamins are not present, SAM may not break down properly. As a consequence, its full benefits will not be obtained, and homocysteine may increase to unsafe levels. Small studies have not shown a consistent effect of SAM on homocysteine levels, but more research is needed.[25][26]
High levels of homocysteine have been associated with atherosclerosis (hardening and narrowing of the arteries), as well as an increased risk of heart attacks, strokes, liver damage, and possibly Alzheimer's disease. Therefore, vitamin B supplements are often taken along with SAM. These vitamins help metabolize the homocysteine into other useful compounds.[27]
Another reported side effect of SAM is insomnia; therefore, the supplement is often taken in the morning.[23] Other reports of mild side effects include lack of appetite, constipation, nausea, dry mouth, sweating, and anxiety/nervousness, but in placebo-controlled studies, these side effects occur at about the same incidence in the placebo groups. Some users report increased anxiety with as little as 50 mg/day.[28]
Therapeutic doses range from 400 mg/day to 1600 mg/day, although higher doses are used in some cases.[19][29] Some physicians recommend lower doses, ranging from 50 to 200 mg/day, to treat mild depression without triggering negative side effects.[28]
Induction of mania
In an extensive MEDLINE search on SAM, Kagan found induction of mania in one patient out of 15 treated with parenteral SAM. In the same review, Lipinski found the apparent induction of mania in two patients with bipolar disorder (total of nine depressed patients studied).[30] Both depression and mania can be life-threatening conditions that may cause cognitive dysfunction even after remission.[31] There is concern that antidepressants in general can induce mania or hypomania in bipolar persons.[32]
Interactions and contraindications
- SAM reduces insulin resistance.[33] This may lead to hypoglycemia when used with antidiabetic drugs.
See also
- DNA methyltransferase
- SAM riboswitch
References
- ^ a b Cantoni, GL (1952). "The Nature of the Active Methyl Donor Formed Enzymatically from L-Methionine and Adenosinetriphosphate". J Am Chem Soc 74 (11): 2942–3. doi:10.1021/ja01131a519.
- ^ Finkelstein J, Martin J (2000). "Homocysteine". Int J Biochem Cell Biol 32 (4): 385–9. doi:10.1016/S1357-2725(99)00138-7. PMID 10762063.
- ^ Födinger M, Hörl W, Sunder-Plassmann G (Jan-February 2000). "Molecular biology of 5,10-methylenetetrahydrofolate reductase". J Nephrol 13 (1): 20–33. PMID 10720211.
- ^ Booker, SJ; Grove, TL (2010). "Mechanistic and functional versatility of radical SAM enzymes". F1000 biology reports 2: 52. doi:10.3410/B2-52. PMC 2996862. PMID 21152342. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2996862.
- ^ Roje S (2006). "S-Adenosyl-L-methionine: beyond the universal methyl group donor". Phytochemistry 67 (15): 1686–98. doi:10.1016/j.phytochem.2006.04.019. PMID 16766004.
- ^ Loenen W (2006). "S-adenosylmethionine: jack of all trades and master of everything?". Biochem Soc Trans 34 (Pt 2): 330–3. doi:10.1042/BST20060330. PMID 16545107.
- ^ Chiang P, Gordon R, Tal J, Zeng G, Doctor B, Pardhasaradhi K, McCann P (1996). "S-Adenosylmethionine and methylation". FASEB J 10 (4): 471–80. PMID 8647346.
- ^ "Investigating SAM-e". Geriatric Times. 2001. http://www.geriatrictimes.com/g010923.html. Retrieved 2006-12-08.
- ^ Kagan, BL; Sultzer, DL; Rosenlicht, N; Gerner, RH (May 1, 1990). "Oral S-adenosylmethionine in depression: a randomized, double-blind, placebo-controlled trial". Am J Psychiatry 147 (5): 591–5. PMID 2183633. http://www.ajp.psychiatryonline.org/cgi/content/abstract/147/5/591. Retrieved 2007-02-16.
- ^ Rosenbaum, JF; Fava, M; Falk, WE; Pollack, MH; Cohen, LS; Cohen, BM; Zubenko, GS (May 1990). "The antidepressant potential of oral S-adenosyl-l-methionine". Acta Psychiatrica Scandinavica 81 (5): 432–6. doi:10.1111/j.1600-0447.1990.tb05476.x. PMID 2113347.
- ^ S-Adenosyl-L-Methionine for Treatment of Depression, Osteoarthritis, and Liver Disease, Agency for Healthcare Research and Quality (Department of Health and Human Services)
- ^ Bottiglieri T, Godfrey P, Flynn T, Carney MW, Toone BK, Reynolds EH. (1990). "Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine". J Neurol Neurosurg Psychiatry 53 (12): 1096–8. doi:10.1136/jnnp.53.12.1096. PMC 488323. PMID 2292704. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=488323.
- ^ Morrison LD, Smith DD, Kish SJ. (1996). "Brain S-adenosylmethionine levels are severely decreased in Alzheimer's disease". J Neurochem. 67 (3): 1328–31. doi:10.1046/j.1471-4159.1996.67031328.x. PMID 8752143.
- ^ Bottiglieri T. (1997). "Ademetionine (S-adenosylmethionine) neuropharmacology: implications for drug therapies in psychiatric and neurological disorders". Expert Opin Investig Drugs. 6 (4): 417–26.. doi:10.1517/13543784.6.4.417. PMID 15989609.
- ^ Tchantchou F, Graves M, Ortiz D, Chan A, Rogers E, Shea TB. (2006). "S-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease" (PDF). J Nutr Health Aging. 10 (6): 541–4. PMID 17183426. http://greengene.uml.edu/publish/publications/SAMLink.pdf.
- ^ David Mischoulon & Maurizio Fava. ""Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence"". http://www.ajcn.org/content/76/5/1158S.full.pdf.
- ^ Geoffrey Cowley & Anne Underwood. ""What is SAMe"". http://biopsychiatry.com/sameart.html.
- ^ ""SAMe"". mayoclinic. http://www.mayoclinic.com/health/same/NS_patient-same/DSECTION=evidence.
- ^ a b c d Najm WI, Reinsch S, Hoehler F, Tobis JS, Harvey PW (February 2004). "S-Adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis symptoms: A double-blind cross-over trial. ISRCTN36233495". BMC Musculoskelet Disord 5: 6. doi:10.1186/1471-2474-5-6. PMC 387830. PMID 15102339. http://www.biomedcentral.com/1471-2474/5/6.
- ^ a b c "S-Adenosylmethionine (SAMe)". University of Maryland Medical Center. 2004. http://www.umm.edu/altmed/articles/s-adenosylmethionine-000324.htm. Retrieved 2009-11-09.
- ^ "Product Review: SAMe". ConsumerLab. 2003-11-18. http://www.consumerlab.com/results/same.asp. Retrieved 2006-12-19.
- ^ "What Is SAMe". Newsweek. July 1999. http://www.newsweek.com/1999/07/04/what-is-same.html. Retrieved 2010-08-30.
- ^ a b "SAMe (S-adenosylmethionine)". About.com. http://www.wholehealthmd.com/ME2/dirmod.asp?nm=Reference+Library&type=AWHN_Supplements&id=E5789DDA2807440687228DC727CDF39C&tier=2. Retrieved 2006-12-07.
- ^ Rydberg B, Lindahl T (1982). "Nonenzymatic methylation of DNA by the intracellular methyl group donor S-adenosyl-L-methionine is a potentially mutagenic reaction". EMBO J. 1 (2): 211–6. PMC 553022. PMID 7188181. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=553022.
- ^ drweil.com. "Dr. Weil: Can SAM-e hurt my heart?". http://www.drweil.com/drw/u/QAA400465/Can-SAMe-Hurt-My-Heart.html.
- ^ Thompson MA, Bauer BA, Loehrer LL et al. (May 2009). "Dietary supplement S-adenosyl-L-methionine (AdoMet) effects on plasma homocysteine levels in healthy human subjects: a double-blind, placebo-controlled, randomized clinical trial". J Altern Complement Med 15 (5): 523–9. doi:10.1089/acm.2008.0402. PMC 2875864. PMID 19422296. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2875864.
- ^ "SAM-e & homocysteine". www.nutraseal.com. Archived from the original on 2007-09-28. http://web.archive.org/web/20070928050935/http://www.nutraseal.com/index.asp?PageAction=Custom&ID=56#function. Retrieved 2007-06-04.
- ^ a b Ray Sahelian, M.D. (2009-05-05). "SAM-e supplement benefits for depression and side effects by Ray Sahelian, M.D., mood, liver, and arthritis, dosage 100mg, 200mg". http://www.raysahelian.com/sam-e.html. Retrieved 2009-05-05.
- ^ Mischoulon, D; Fava, M (November 2002). "Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence" (PDF). Am J Clin Nutr 76 (5): 1158S–61S. PMID 12420702. http://www.ajcn.org/cgi/reprint/76/5/1158S.pdf. Retrieved 2006-12-07.
- ^ Janicak PG, Lipinski J, Davis JM, Altman E, Sharma RP (1989). "Parenteral S-adenosyl-methionine (SAMe) in depression: literature review and preliminary data". Psychopharmacology bulletin 25 (2): 238–42. PMID 2690166.
- ^ Jamison, Kay (Updated January 21, 2004). "Brain Damage in Depression and Bipolar Disorder". McMan's Depression and Bipolar Web. http://www.mcmanweb.com/article-161.htm.
- ^ "Antidepressants in Bipolar Disorder: The Controversies". PsychEducation.org. November 2006. http://www.psycheducation.org/bipolar/controversy.htm. Retrieved 2007-04-10.
- ^ "S-Adenosyl-L-Methionine Increases Skeletal Muscle Mitochondrial DNA Density and Whole Body Insulin Sensitivity in OLETF Rats1". http://jn.nutrition.org/content/137/2/339.short.
External links
- EINECS number 249-946-8
- Shippy, R Andrew; Mendez, Douglas; Jones, Kristina; Cergnul, Irene; Karpiak, Stephen E (2004). "S-adenosylmethionine (SAM-e) for the treatment of depression in people living with HIV/AIDS". BMC Psychiatry 4: 38. doi:10.1186/1471-244X-4-38. PMC 535560. PMID 15538952. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=535560.
- About.com SAM-e Resource Index at About.com
- list of known SAM-e drug interactions and precautions in use at University of Maryland Medical Centers
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Enzyme cofactors
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| Active forms |
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vitamins
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TPP / ThDP (B1) · FMN, FAD (B2) · NAD+, NADH, NADP+, NADPH (B3) · Coenzyme A (B5) · PLP / P5P (B6) · Biotin (B7) · THFA / H4FA, DHFA / H2FA, MTHF (B9) · AdoCbl, MeCbl (B12) · Ascorbic Acid (C) · Phylloquinone (K1), Menaquinone (K2) · Coenzyme F420
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non-vitamins
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ATP · CTP · SAMe · PAPS · GSH · Coenzyme B · Cofactor F430 · Coenzyme M · Coenzyme Q · Heme / Haem (A, B, C, O) · Lipoic Acid · Methanofuran · Molybdopterin/Molybdenum cofactor · PQQ · THB / BH4 · THMPT / H4MPT
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minerals
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Ca2+ · Cu2+ · Fe2+, Fe3+ · Mg2+ · Mn2+ · Mo · Ni2+ · Se · Zn2+
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| Base forms |
vitamins: see vitamins
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noco, nuvi, sysi/epon, met
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Amino acid metabolism metabolic intermediates
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| K→acetyl-CoA |
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lysine→
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- Saccharopine
- Allysine
- α-Aminoadipic acid
- α-Aminoadipate
- Glutaryl-CoA
- Glutaconyl-CoA
- Crotonyl-CoA
- β-Hydroxybutyryl-CoA
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leucine→
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- α-Ketoisocaproic acid
- Isovaleryl-CoA
- 3-Methylcrotonyl-CoA
- 3-Methylglutaconyl-CoA
- HMG-CoA
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tryptophan→alanine→
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- N'-Formylkynurenine
- Kynurenine
- Anthranilic acid
- 3-Hydroxykynurenine
- 3-Hydroxyanthranilic acid
- 2-Amino-3-carboxymuconic semialdehyde
- 2-Aminomuconic semialdehyde
- 2-Aminomuconic acid
- Glutaryl-CoA
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| G |
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G→pyruvate→citrate
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glycine→serine→
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- glycine→creatine: Glycocyamine
- Phosphocreatine
- Creatinine
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G→glutamate→
α-ketoglutarate
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histidine→
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- Urocanic acid
- Imidazol-4-one-5-propionic acid
- Formiminoglutamic acid
- Glutamate-1-semialdehyde
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proline→
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- 1-Pyrroline-5-carboxylic acid
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arginine→
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- Ornithine
- Putrescine
- Agmatine
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other
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- cysteine+glutamate→glutathione: γ-Glutamylcysteine
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G→propionyl-CoA→
succinyl-CoA
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valine→
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- α-Ketoisovaleric acid
- Isobutyryl-CoA
- Methacrylyl-CoA
- 3-Hydroxyisobutyryl-CoA
- 3-Hydroxyisobutyric acid
- 2-Methyl-3-oxopropanoic acid
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isoleucine→
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- 2,3-Dihydroxy-3-methylpentanoic acid
- 2-Methylbutyryl-CoA
- Tiglyl-CoA
- 2-Methylacetoacetyl-CoA
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methionine→
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- generation of homocysteine: S-Adenosyl methionine
- S-Adenosyl-L-homocysteine
- Homocysteine
- conversion to cysteine: Cystathionine
- alpha-Ketobutyric acid+Cysteine
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threonine→
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propionyl-CoA→
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G→fumarate
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phenylalanine→tyrosine→
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- 4-Hydroxyphenylpyruvic acid
- Homogentisic acid
- 4-Maleylacetoacetate
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G→oxaloacetate
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| Other |
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mt, k, c/g/r/p/y/i, f/h/s/l/o/e, a/u, n, m
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k, cgrp/y/i, f/h/s/l/o/e, au, n, m, epon
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m(A16/C10),i(k, c/g/r/p/y/i, f/h/s/o/e, a/u, n, m)
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biochemical families: proteins (amino acids/intermediates) · nucleic acids (constituents/intermediates) · carbohydrates (glycoproteins, alcohols, glycosides)
lipids (fatty acids/intermediates, phospholipids, steroids, sphingolipids, eicosanoids) · tetrapyrroles/intermediates
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