| Drug Name: | Dehydrated Alcohol (64-17-5) |
|---|---|
| PubChem ID: | 702 |
| SMILES: | CCO |
| InchiKey: | LFQSCWFLJHTTHZ-UHFFFAOYSA-N |
| Therapeutic Category: | Anti-Infective Agents, Central Nervous System Agents, Central Nervous System Depressants, Solvents |
| Molecular Weight (dalton) | : | 46.069 |
| LogP | : | -0.0014 |
| Ring Count | : | 0 |
| Hydrogen Bond Acceptor Count | : | 1 |
| Hydrogen Bond Donor Count | : | 1 |
| Total Polar Surface Area | : | 20.23 |
This panel provides information on interacting drugs and their ADRs along with references
| Interacting drug | Toxicity | Interaction Type | Mechanism | Reference |
|---|
This panel provides drug-protein interaction and their ADRs along with references
| Toxicity | Interacting Protein | Mechanism | Reference |
|---|---|---|---|
| Alcohol Abuse | Serotransferrin (P02787) | Carbohydrate-deficient transferrin proves to be the best marker of alcohol abuse because it allows objective detection, so that therapeutic action can be started early, which is easier and more effective than in alcohol dependence. [ ADR Type 3 ] | Objective diagnosis of alcohol abuse: compared values of carbohydrate-deficient transferrin (CDT), gamma-glutamyl transferase (GGT), and mean corpuscular volume |
| Alcohol Intoxication | gamma-aminobutyric acid (GABA) receptors (Q5TZ16) | Positive modulators for the GABA(A) receptor (20 mg/kg 3alpha-hydroxy-5alpha-pregnan-20-one and 10-30 mg/kg chlordiazepoxide) and opioid receptor (10 mg/kg morphine) produced significant elevations on Edinger-Westphal c-Fos expression@showing that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication [ ADR Type 1 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Alcohol Intoxication | Mitogen-activated protein kinase(ERK) (P28482) | Lockade of ERK 1/2 phosphorylation with the mitogen-activated protein kinase (MEK) 1/2 inhibitor SL327 blocked alcohol-induced c-Fos expression@showing that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication [ ADR Type 2 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Alcohol Intoxication | Opioid growth factor receptor (Q9NZT2) | Positive modulators for the GABA(A) receptor (20 mg/kg 3alpha-hydroxy-5alpha-pregnan-20-one and 10-30 mg/kg chlordiazepoxide) and opioid receptor (10 mg/kg morphine) produced significant elevations on Edinger-Westphal c-Fos expression@showing that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication [ ADR Type 1 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Alcohol Intoxication | Proto-oncogene protein c-fos (P01100) | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus through activation of the MEK1/2-ERK1/2-Stat3 pathway,showing that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication [ ADR Type 2 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Alcohol Intoxication | Signal transducer and activator of transcription 3 (P40763) | Time-dependent increases in phospho-extracellular signal-regulated kinase (ERK) 1/2 were found to occur simultaneously with increases in serine 727 phospho-Stat3 [ ADR Type 2 ] | Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms |
| Apap Toxicity | Cytochrome P450 2E1 (P05181) | APAP toxicity is increased in both humans and rodents by pretreatment with various inducers of CYP gene expression@ including ethanol@ an inducer of CYP2E and CYP3A isoforms (12@ 13)@ and phenobarbital (PB)@ a well-known inducer of CYP2B@ CYP3A@ and other isoforms. [ ADR Type 4 ] | Toxicology Protecting liver from painkiller's lethal dose |
| Apap Toxicity | Cytochrome P450 3A4 (P08684) | APAP toxicity is increased in both humans and rodents by pretreatment with various inducers of CYP gene expression@ including ethanol@ an inducer of CYP2E and CYP3A isoforms (12@ 13)@ and phenobarbital (PB)@ a well-known inducer of CYP2B@ CYP3A@ and other isoforms [ ADR Type 4 ] | Toxicology Protecting liver from painkiller's lethal dose |
| Delay Puberty | growth hormone (GH) (P10912) | Alcohol (ALC) delays puberty in female rats and alters the development of a normal menstrual pattern in rhesus monkeys These actions are associated with depressed serum levels of growth hormone (GH)@ luteinizing hormone and insulin-like growth factor-1 (IGF-1) Ability of ALC to supress prepubertal IGF1 gene expression can also occur independently of any alterations in the level of circulating GH [ ADR Type 1 ] | Alcohol suppresses insulin-like growth factor-1 gene expression in prepubertal transgenic female mice overexpressing the bovine growth hormone gene |
| Delay Puberty | Insulin-like growth factor-1 receptor (Q6QHH2) | Alcohol (ALC) delays puberty in female rats and alters the development of a normal menstrual pattern in rhesus monkeys These actions are associated with depressed serum levels of growth hormone (GH)@ luteinizing hormone and insulin-like growth factor-1 (IGF-1) Ability of ALC to supress prepubertal IGF1 gene expression can also occur independently of any alterations in the level of circulating GH [ ADR Type 1 ] | Alcohol suppresses insulin-like growth factor-1 gene expression in prepubertal transgenic female mice overexpressing the bovine growth hormone gene |
| Delirium | Cannabinoid receptor (Q71SP5) | The homozyGOus genotype CNR1 1359A/A confers vulnerability to alcohol withdrawal delirium [ ADR Type 3 ] | Association of a CB1 cannabinoid receptor gene (CNR1) polymorphism with severe alcohol dependence Drug Alcohol |
| Hyperparathyroidism | Parathyroid hormone (Q03431) | The changes in parathyroid hormone are not consistent and since there is no greater incidence of hyperparathyroidism in alcoholic patients@ it SUGGESTS that alcohol does not have a long-term effect on the parathyroid glands. [ ADR Type 1 ] | Alcohol and bone disease Alcohol |
| Impair Liver Regeneration | glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (P04406) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA),suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impair Liver Regeneration | Insulin receptor substrate 1 (P35568) | Ethanol treatment caused 30 to 50% reductions in the levels of tyrosyl phosphorylation of IRS-1@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impair Liver Regeneration | Insulin receptor substrate 2 (Q9Y4H2) | Ethanol treatment caused insulin-stimulated tyrosyl phosphorylation of the insulin receptor beta-subunit@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impair Liver Regeneration | Mitogen-activated protein kinase(ERK) (P28482) | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impair Liver Regeneration | Phosphatidylinositol-4-phosphate 3-kinase (O00443) | Ethanol treatment is associated with phosphatidylinositol-3 kinase with tyrosyl-phosphorylated IRS-1, and MAP kinase and phosphatidylinositol-3 kinase activities,suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impair Liver Regeneration | Proliferating cell nuclear antigen (Q00268) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA)@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Impairs Insulin | Eukaryotic translation initiation factor 4E (P06730) | EtOH altered the distribution of eukaryotic initiation factor (eIF)4E@ as evidenced by a decreased amount of active eIF4E. eIF4G complex@ an increased amount of inactive eIF4E-binding protein (BP)1 complex@ and decreased 4E-BP1 phosphorylation@which impairs insulin and IGF-I stimulation of S6K1. [ ADR Type 2 ] | Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle |
| Impairs Insulin | Eukaryotic translation initiation factor 4E-binding protein (Q13541) | EtOH altered the distribution of eukaryotic initiation factor (eIF)4E@ as evidenced by a decreased amount of active eIF4E. eIF4G complex@ an increased amount of inactive eIF4E-binding protein (BP)1 complex@ and decreased 4E-BP1 phosphorylation@which impairs insulin and IGF-I stimulation of S6K1. [ ADR Type 2 ] | Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle |
| Impairs Insulin | Insulin (P01308) | EtOH altered the distribution of eukaryotic initiation factor (eIF)4E, as evidenced by a decreased amount of active eIF4E eIF4G complex, an increased amount of inactive eIF4E-binding protein (BP)1 complex, and decreased 4E-BP1 phosphorylation,which impairs insulin and IGF-I stimulation of S6K1 [ ADR Type 2 ] | Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle |
| Impairs Insulin | Insulin-like growth factor I (P05017) | EtOH altered the distribution of eukaryotic initiation factor (eIF)4E@ as evidenced by a decreased amount of active eIF4E eIF4G complex@ an increased amount of inactive eIF4E-binding protein (BP)1 complex@ and decreased 4E-BP1 phosphorylation@which impairs insulin and IGF-I stimulation of S6K1 [ ADR Type 2 ] | Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle |
| Impairs Insulin | Ribosomal protein S6-1 (O48549) | A reduction in the phosphorylation of the ribosomal protein S6 after treatment of alcohol(EtOH),which impairs insulin and IGF-I stimulation of S6K1 [ ADR Type 2 ] | Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle |
| Inhibit Dna Synthesis | glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (P04406) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA),suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Inhibit Dna Synthesis | Insulin receptor substrate 1 (P35568) | Ethanol treatment caused 30 to 50% reductions in the levels of tyrosyl phosphorylation of IRS-1@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Inhibit Dna Synthesis | Insulin receptor substrate 2 (Q9Y4H2) | Ethanol treatment caused insulin-stimulated tyrosyl phosphorylation of the insulin receptor beta-subunit@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Inhibit Dna Synthesis | Mitogen-activated protein kinase(ERK) (P28482) | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Inhibit Dna Synthesis | Phosphatidylinositol-4-phosphate 3-kinase (O00443) | Ethanol treatment is associated with phosphatidylinositol-3 kinase with tyrosyl-phosphorylated IRS-1, and MAP kinase and phosphatidylinositol-3 kinase activities,suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Inhibit Dna Synthesis | Proliferating cell nuclear antigen (Q00268) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA)@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Locomotor Stimulation | Thyrotropin-releasing hormone (TRH) (Q01717) | Ethanol-induced locomotor stimulation in rats after thyrotropin-releasing hormone [ ADR Type 1 ] | Ethanol-induced locomotor stimulation in rats after thyrotropin-releasing hormone |
| Mitochondrial Glutathione Depletion | Mitochondrial 2-oxoglutarate/malate carrier protein (OGCP) (Q02978) | Sensitivity of the 2-oxoglutarate carrier to alcohol intake contributes to mitochondrial glutathione depletion [ ADR Type 1 ] | A role for the 2-oxoglutarate carrier in glutathione transport into hepatocyte mitochondria |
| Mute Cellular Responses To Growth Factor Stimulation | glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (P04406) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA),suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Mute Cellular Responses To Growth Factor Stimulation | Insulin receptor substrate 1 (P35568) | Ethanol treatment caused 30 to 50% reductions in the levels of tyrosyl phosphorylation of IRS-1@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Mute Cellular Responses To Growth Factor Stimulation | Insulin receptor substrate 2 (Q9Y4H2) | Ethanol treatment caused insulin-stimulated tyrosyl phosphorylation of the insulin receptor beta-subunit@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Mute Cellular Responses To Growth Factor Stimulation | Mitogen-activated protein kinase(ERK) (P28482) | Ethanol treatment caused phosphorylation of Erk2@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to Chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation. [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Mute Cellular Responses To Growth Factor Stimulation | Phosphatidylinositol-4-phosphate 3-kinase (O00443) | Ethanol treatment is associated with phosphatidylinositol-3 kinase with tyrosyl-phosphorylated IRS-1, and MAP kinase and phosphatidylinositol-3 kinase activities,suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression,which leads to chronic ethanol toxicity impairs liver regeneration, inhibits DNA synthesis, and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Mute Cellular Responses To Growth Factor Stimulation | Proliferating cell nuclear antigen (Q00268) | Ethanol treatment resulted in 30 to 50% reductions in the expression levels of two important insulin-responsive genes: glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and proliferating cell nuclear antigen (PCNA)@suggesting that ethanol treatment substantially inhibits IRS-1 and MAP kinase signaling and growth-associated gene expression@which leads to chronic ethanol toxicity impairs liver regeneration@ inhibits DNA synthesis@ and mutes cellular responses to growth factor stimulation [ ADR Type 1 ] | Ethanol inhibition of insulin signaling in hepatocellular carcinoma cells |
| Narcosis | Proenkephalin (P01210) | An inhibition of endogenous enkephalin transmission, may significantly inhibit ethanol narcosis in the rat. [ ADR Type 1 ] | The effect of neurotensin, TRH and the delta-opioid receptor antagonist ICI 174864 on alcohol-induced narcosis in rats |
| Osteopenia Aseptic Necrosis | GOnadal hormones (P00020) | The DECREASE in the levels of the GOnadal hormones and the INCREASE of cortisol, observed in chronic alcoholics, may INDIRECTLY cause osteopenia and aseptic necrosis [ ADR Type 1 ] | Alcohol and bone disease Alcohol |
| Pancreatitis | D(2) dopamine receptor (P14416) | Alcohol induced chronic pancreatitis [ ADR Type 1 ] | Male limited association of the dopamine receptor D2 gene TaqI a polymorphism and alcohol dependence |
| Pancreatitis | Glutathione S-transferase Mu 1 (P09488) | GSTM1 null alcohol users@ particularly young female@ are less susceptible to chronic pancreatitis (CP) [ ADR Type 1 ] | Glutathione S-transferase Mu null genotype affords protection against alcohol induced chronic pancreatitis |
| Pancreatitis | Myeloperoxidase precursor (P05164) | Pancreatic tissue and blood samples were assessed for reduced (GSH) and ixidized (GSSG) glutathione@ malondialdehyde@ conjugated dienes (CD)@ and myeloperoxidase@suggesting the influence of ethanol on the pancreatic generation of oxygen-free radicals (OFR) in alcohol-induced acute pancreatitis as one possible pathway of proenzyme activation in this disease [ ADR Type 1 ] | Oxygen radical production precedes alcohol-induced acute pancreatitis in rats |
| Subclinical Pancreatic Damage | Pancreatitis associated protein (Q06141) | Increased serum pancreatitis associated protein (PAP) concentration after longterm alcohol consumption provides further evidence for regular subclinical pancreatic damage after heavy drinking [ ADR Type 1 ] | Increased serum pancreatitis associated protein (PAP) concentration after longterm alcohol consumption: further evidence for regular subclinical pancreatic damage after heavy drinking |
This panel provides drug-food interactions and their ADRs along with references
This panel provides information on metabolites and their ADRs along with references
| Metabolite | Toxicity | Place of Metabolism | Mechanism | Reference |
|---|
This panel provides information on drug category