Ubisol-AquaTM: Coenzyme Q10 prevents antiretroviral toxic neuropathy in an in vitro model

Catherine L Cherry, Masqura Mobarok, Steven Lodewyk Wesselingh, Randi Fain, Shelley Weinstock, Gilda Tachedjian, Seema Srivastava, David P Tyssen, Jonathon D Glass, David J Hooker

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Abstract

BACKGROUND: Peripheral neuropathy is the dose-limiting toxicity of stavudine and didanosine (nucleoside analogs used in HIV treatment) and is attributed to mitochondrial toxicity from these drugs. Acetyl L-carnitine (ALC) and co-enzyme Q(10) are proposed as neuropathy treatments, but evidence to support these is limited. METHODS: We examined ALC and a water-soluble formulation of co-enzyme Q(10) (H(Q)O) for the prevention of d4T and ddI neurotoxicity using cultured fetal rat DRG as an in vitro model. RESULTS: DdI (33microM) and d4T (50microM) caused clear toxicity (impaired neurite growth) by day 8 of DRG culture. H(Q)O at concentrations 1-100microM completely prevented the toxicity of 33microM ddI in vitro and ALC at concentrations 1-100 microM substantially (but incompletely) prevented ddI toxicity in this model. In contrast, ALC was ineffective at all concentrations tested for preventing the toxicity of 50microM d4T. H(Q)O showed dose-dependent efficacy for preventing d4T toxicity. H(Q)O (1microM) partially prevented d4T toxicity while 10 and 100microM H(Q)O completely prevented d4T toxicity in this model. CONCLUSIONS: We find H(Q)O is superior to ALC for preventing the neurotoxicity of d4T (the HIV treatment most associated with neuropathy) and ddI in vitro. Further study is needed to clarify any clinical role for co-enzyme Q(10) co-administration with d4T and ddI and to assess whether this compound may have a role in treating established cases of neuropathy.
Original languageEnglish
Pages (from-to)232 - 239
Number of pages8
JournalCurrent HIV Research
Volume8
Issue number3
DOIs
Publication statusPublished - 2010

Cite this

Cherry, Catherine L ; Mobarok, Masqura ; Wesselingh, Steven Lodewyk ; Fain, Randi ; Weinstock, Shelley ; Tachedjian, Gilda ; Srivastava, Seema ; Tyssen, David P ; Glass, Jonathon D ; Hooker, David J. / Ubisol-AquaTM: Coenzyme Q10 prevents antiretroviral toxic neuropathy in an in vitro model. In: Current HIV Research. 2010 ; Vol. 8, No. 3. pp. 232 - 239.
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abstract = "BACKGROUND: Peripheral neuropathy is the dose-limiting toxicity of stavudine and didanosine (nucleoside analogs used in HIV treatment) and is attributed to mitochondrial toxicity from these drugs. Acetyl L-carnitine (ALC) and co-enzyme Q(10) are proposed as neuropathy treatments, but evidence to support these is limited. METHODS: We examined ALC and a water-soluble formulation of co-enzyme Q(10) (H(Q)O) for the prevention of d4T and ddI neurotoxicity using cultured fetal rat DRG as an in vitro model. RESULTS: DdI (33microM) and d4T (50microM) caused clear toxicity (impaired neurite growth) by day 8 of DRG culture. H(Q)O at concentrations 1-100microM completely prevented the toxicity of 33microM ddI in vitro and ALC at concentrations 1-100 microM substantially (but incompletely) prevented ddI toxicity in this model. In contrast, ALC was ineffective at all concentrations tested for preventing the toxicity of 50microM d4T. H(Q)O showed dose-dependent efficacy for preventing d4T toxicity. H(Q)O (1microM) partially prevented d4T toxicity while 10 and 100microM H(Q)O completely prevented d4T toxicity in this model. CONCLUSIONS: We find H(Q)O is superior to ALC for preventing the neurotoxicity of d4T (the HIV treatment most associated with neuropathy) and ddI in vitro. Further study is needed to clarify any clinical role for co-enzyme Q(10) co-administration with d4T and ddI and to assess whether this compound may have a role in treating established cases of neuropathy.",
author = "Cherry, {Catherine L} and Masqura Mobarok and Wesselingh, {Steven Lodewyk} and Randi Fain and Shelley Weinstock and Gilda Tachedjian and Seema Srivastava and Tyssen, {David P} and Glass, {Jonathon D} and Hooker, {David J}",
year = "2010",
doi = "10.2174/157016210791111106",
language = "English",
volume = "8",
pages = "232 -- 239",
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Cherry, CL, Mobarok, M, Wesselingh, SL, Fain, R, Weinstock, S, Tachedjian, G, Srivastava, S, Tyssen, DP, Glass, JD & Hooker, DJ 2010, 'Ubisol-AquaTM: Coenzyme Q10 prevents antiretroviral toxic neuropathy in an in vitro model', Current HIV Research, vol. 8, no. 3, pp. 232 - 239. https://doi.org/10.2174/157016210791111106

Ubisol-AquaTM: Coenzyme Q10 prevents antiretroviral toxic neuropathy in an in vitro model. / Cherry, Catherine L; Mobarok, Masqura; Wesselingh, Steven Lodewyk; Fain, Randi; Weinstock, Shelley; Tachedjian, Gilda; Srivastava, Seema; Tyssen, David P; Glass, Jonathon D; Hooker, David J.

In: Current HIV Research, Vol. 8, No. 3, 2010, p. 232 - 239.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Ubisol-AquaTM: Coenzyme Q10 prevents antiretroviral toxic neuropathy in an in vitro model

AU - Cherry, Catherine L

AU - Mobarok, Masqura

AU - Wesselingh, Steven Lodewyk

AU - Fain, Randi

AU - Weinstock, Shelley

AU - Tachedjian, Gilda

AU - Srivastava, Seema

AU - Tyssen, David P

AU - Glass, Jonathon D

AU - Hooker, David J

PY - 2010

Y1 - 2010

N2 - BACKGROUND: Peripheral neuropathy is the dose-limiting toxicity of stavudine and didanosine (nucleoside analogs used in HIV treatment) and is attributed to mitochondrial toxicity from these drugs. Acetyl L-carnitine (ALC) and co-enzyme Q(10) are proposed as neuropathy treatments, but evidence to support these is limited. METHODS: We examined ALC and a water-soluble formulation of co-enzyme Q(10) (H(Q)O) for the prevention of d4T and ddI neurotoxicity using cultured fetal rat DRG as an in vitro model. RESULTS: DdI (33microM) and d4T (50microM) caused clear toxicity (impaired neurite growth) by day 8 of DRG culture. H(Q)O at concentrations 1-100microM completely prevented the toxicity of 33microM ddI in vitro and ALC at concentrations 1-100 microM substantially (but incompletely) prevented ddI toxicity in this model. In contrast, ALC was ineffective at all concentrations tested for preventing the toxicity of 50microM d4T. H(Q)O showed dose-dependent efficacy for preventing d4T toxicity. H(Q)O (1microM) partially prevented d4T toxicity while 10 and 100microM H(Q)O completely prevented d4T toxicity in this model. CONCLUSIONS: We find H(Q)O is superior to ALC for preventing the neurotoxicity of d4T (the HIV treatment most associated with neuropathy) and ddI in vitro. Further study is needed to clarify any clinical role for co-enzyme Q(10) co-administration with d4T and ddI and to assess whether this compound may have a role in treating established cases of neuropathy.

AB - BACKGROUND: Peripheral neuropathy is the dose-limiting toxicity of stavudine and didanosine (nucleoside analogs used in HIV treatment) and is attributed to mitochondrial toxicity from these drugs. Acetyl L-carnitine (ALC) and co-enzyme Q(10) are proposed as neuropathy treatments, but evidence to support these is limited. METHODS: We examined ALC and a water-soluble formulation of co-enzyme Q(10) (H(Q)O) for the prevention of d4T and ddI neurotoxicity using cultured fetal rat DRG as an in vitro model. RESULTS: DdI (33microM) and d4T (50microM) caused clear toxicity (impaired neurite growth) by day 8 of DRG culture. H(Q)O at concentrations 1-100microM completely prevented the toxicity of 33microM ddI in vitro and ALC at concentrations 1-100 microM substantially (but incompletely) prevented ddI toxicity in this model. In contrast, ALC was ineffective at all concentrations tested for preventing the toxicity of 50microM d4T. H(Q)O showed dose-dependent efficacy for preventing d4T toxicity. H(Q)O (1microM) partially prevented d4T toxicity while 10 and 100microM H(Q)O completely prevented d4T toxicity in this model. CONCLUSIONS: We find H(Q)O is superior to ALC for preventing the neurotoxicity of d4T (the HIV treatment most associated with neuropathy) and ddI in vitro. Further study is needed to clarify any clinical role for co-enzyme Q(10) co-administration with d4T and ddI and to assess whether this compound may have a role in treating established cases of neuropathy.

UR - http://www.ncbi.nlm.nih.gov/pubmed/20158454

U2 - 10.2174/157016210791111106

DO - 10.2174/157016210791111106

M3 - Article

VL - 8

SP - 232

EP - 239

JO - Current HIV Research

JF - Current HIV Research

SN - 1570-162X

IS - 3

ER -