Effects of Disulfiram and Pyridoxine on Serum Cholesterol

Major, Leslie F.; Goyer, Peter F.

doi:10.7326/0003-4819-88-1-53

Cited by 18 publications

(2 citation statements)

References 20 publications

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“…Importantly, drugs that specifically target the protein product of ALDH2 , used to treat alcohol dependence, such as disulfiram, should be further investigated for their effect on LDL-C and CAD risk. Preliminary studies suggest that disulfiram increases total cholesterol (Major and Goyer 1978 ), thus the drug may associate with a reduction in risk of CAD (in keeping with the expected pattern of association as reported in Table 2 ). The association of PLG with LDL-C and CAD is interesting: prospective studies and clinical trials show consistent associations of plasminogen with lipid levels (Crutchley et al 1989 ) and CAD risk (Baigent et al 1998 ; Lowe et al 2004 ; Sakkinen et al 1999 ).…”

Section: Discussionsupporting

confidence: 74%

Harnessing publicly available genetic data to prioritize lipid modifying therapeutic targets for prevention of coronary heart disease based on dysglycemic risk

et al. 2016

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Therapeutic interventions that lower LDL-cholesterol effectively reduce the risk of coronary artery disease (CAD). However, statins, the most widely prescribed LDL-cholesterol lowering drugs, increase diabetes risk. We used genome-wide association study (GWAS) data in the public domain to investigate the relationship of LDL-C and diabetes and identify loci encoding potential drug targets for LDL-cholesterol modification without causing dysglycemia. We obtained summary-level GWAS data for LDL-C from GLGC, glycemic traits from MAGIC, diabetes from DIAGRAM and CAD from CARDIoGRAMplusC4D consortia. Mendelian randomization analyses identified a one standard deviation (SD) increase in LDL-C caused an increased risk of CAD (odds ratio [OR] 1.63 (95 % confidence interval [CI] 1.55, 1.71), which was not influenced by removing SNPs associated with diabetes. LDL-C/CAD-associated SNPs showed consistent effect directions (binomial P = 6.85 × 10−5). Conversely, a 1-SD increase in LDL-C was causally protective of diabetes (OR 0.86; 95 % CI 0.81, 0.91), however LDL-cholesterol/diabetes-associated SNPs did not show consistent effect directions (binomial P = 0.15). HMGCR, our positive control, associated with LDL-C, CAD and a glycemic composite (derived from GWAS meta-analysis of four glycemic traits and diabetes). In contrast, PCSK9, APOB, LPA, CETP, PLG, NPC1L1 and ALDH2 were identified as “druggable” loci that alter LDL-C and risk of CAD without displaying associations with dysglycemia. In conclusion, LDL-C increases the risk of CAD and the relationship is independent of any association of LDL-C with diabetes. Loci that encode targets of emerging LDL-C lowering drugs do not associate with dysglycemia, and this provides provisional evidence that new LDL-C lowering drugs (such as PCSK9 inhibitors) may not influence risk of diabetes.Electronic supplementary materialThe online version of this article (doi:10.1007/s00439-016-1647-9) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 74%

Harnessing publicly available genetic data to prioritize lipid modifying therapeutic targets for prevention of coronary heart disease based on dysglycemic risk

et al. 2016

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“…The curative group showed a significant reduction in the serum cholesterol level compared to the toxicant control group, while the prophylactic group showed a lower but not significant difference in the serum cholesterol level compared to the toxicant control group in rats that were sacrificed a day after the last dose of LIV and CCl 4 as the case may be for each group. The decrease in cholesterol level in the treated groups relative to the toxicant control group could have been due to phosphatidylcholine [18] and vitamin B 6 [19] present in LIV, because both constituents have been reported to lower blood cholesterol level.…”

Section: Discussionmentioning

confidence: 96%

Protective and curative effects of Livolin forte on carbon tetrachloride-induced liver damage in Wistar rats

Olukiran¹,

Akomolafe²,

Bamitale³

et al. 2014

J Exp Integr Med

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Objective: Livolin forte ® (LIV) is a hepatoprotective drug that is being used in hospitals worldwide in the treatment and management of liver diseases. However, as it appear through the available published literature, the physiological effects of the drug on the liver using a rat model of hepatotoxicity is not yet well established. This study assessed the curative and prophylactic effects of LIV on carbon tetrachloride (CCl4) induced liver damage in rats. Methods: Twenty-four adult Wistar rats were randomly divided into four groups: group I (normal control) received 0.3 ml/kg/day of propylene glycol for one month; group II (toxicant control) was given 0.7 ml/kg/day of CCl4 dissolved in olive oil (1:1, v/v) orally for 7 days; group III received 5.2 mg/kg/day of LIV for one month followed by CCl4 for one week; group IV received CCl4 for one week and subsequently LIV (5.2 mg/kg/day) was administered for one month. Half of the rats were sacrificed one day after the last treatment, the other half after a 2-week recovery period. Results: The toxicant control group had significantly higher AST and ALT activities, total bilirubin and lower total protein and GSH levels compared to the normal control rats. Similarly, significant increase in serum activities of AST and ALT were observed in group III compared to the normal control rats a day after the last treatment with CCl4, whereas after the recovery period no significant differences were observed in nearly all the parameters. Moreover, group IV showed no significant differences in the parameters mentioned above compared to the normal control rats a day after the last treatment with LIV and after the recovery period. Conclusion: The results of this study indicated that LIV was better as a curative agent rather than a prophylactic agent in rats.

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Disulfiram [MAK Value Documentation in German language, 1997]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 24. Lieferung, Ausgabe 1997 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Wirkungsmechanismus Toxikokinetik und Metabolismus Erfahrungen beim Menschen Einmalige Exposition Wiederholte Exposition Wirkung auf Haut und Schleimhäute Allergene Wirkung Reproduktionstoxizität Genotoxizität Kanzerogenität Tierexperimentelle Befunde und In‐vitro‐Untersuchungen Akute Toxizität Subakute, subchronische und chronische Toxizität Wirkung auf Haut und Schleimhäute Allergene Wirkung Reproduktionstoxizität Genotoxizität Kanzerogenität Sonstige Wirkungen Bewertung

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Effects of Disulfiram and Pyridoxine on Serum Cholesterol

Cited by 18 publications

References 20 publications

Harnessing publicly available genetic data to prioritize lipid modifying therapeutic targets for prevention of coronary heart disease based on dysglycemic risk

Harnessing publicly available genetic data to prioritize lipid modifying therapeutic targets for prevention of coronary heart disease based on dysglycemic risk

Protective and curative effects of Livolin forte on carbon tetrachloride-induced liver damage in Wistar rats

Disulfiram [MAK Value Documentation in German language, 1997]

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