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Study · Animal study (in vivo) · caenorhabditis elegans · 2016

8 results

NAD+ Supplementation Attenuates Methylmercury Dopaminergic and Mitochondrial Toxicity in Caenorhabditis Elegans.

Caito SW, Aschner M

Toxicological sciences : an official journal of the Society of Toxicology10 Feb 2016Cited by 33 (Europe PMC)

PMID26865665 (opens in a new tab)PMCIDPMC4914800 (opens in a new tab)DOI10.1093/toxsci/kfw030 (opens in a new tab)PepBankPUB-26865665
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study8

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In worms, NAD+ supplementation before methylmercury prevented cellular NAD+ depletion.

    In plain wordsIn worms, NAD+ supplementation prevented NAD+ depletion compared with methylmercury exposure without supplementation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreasePrevention of cellular NAD depletion
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Comparator
    MeHg exposure without NAD supplementation
    Outcome group
    Mitochondrial function · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Worms treated with MeHg showed depletion in cellular NAD( + )levels, which was prevented by NAD( + )supplementation prior to MeHg treatment.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In worms, NAD+ supplementation prevented methylmercury-induced dopaminergic neurodegeneration.

    In plain wordsIn worms, NAD+ prevented dopamine neuron damage compared with methylmercury exposure without supplementation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseDopaminergic neurodegeneration
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Comparator
    MeHg exposure without NAD supplementation
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD( + )supplementation also prevented DAergic neurodegeneration and deficits in DAergic-dependent behavior upon MeHg exposure.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In worms, NAD+ supplementation prevented dopaminergic-dependent behavioral deficits after methylmercury exposure.

    In plain wordsIn worms, NAD+ prevented behavioral deficits compared with methylmercury exposure without supplementation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseDopaminergic-dependent behavioral deficits
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Comparator
    MeHg exposure without NAD supplementation
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD( + )supplementation also prevented DAergic neurodegeneration and deficits in DAergic-dependent behavior upon MeHg exposure.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In wildtype worms, NAD+ supplementation protected against methylmercury-induced oxidative stress.

    In plain wordsIn wildtype worms, NAD+ reduced oxidative stress compared with methylmercury exposure without supplementation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseOxidative stress
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Comparator
    MeHg exposure without NAD supplementation
    Outcome group
    Mitochondrial function · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In wildtype worms, NAD( + )supplementation provided protection from MeHg-induced oxidative stress and mitochondrial dysfunction.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In wildtype worms, NAD+ supplementation protected against methylmercury-induced mitochondrial dysfunction.

    In plain wordsIn wildtype worms, NAD+ protected mitochondria compared with methylmercury exposure without supplementation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseMitochondrial dysfunction
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Comparator
    MeHg exposure without NAD supplementation
    Outcome group
    Mitochondrial function · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In wildtype worms, NAD( + )supplementation provided protection from MeHg-induced oxidative stress and mitochondrial dysfunction.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 06AnimalEndogenous levelAnimal study (in vivo)Other

    In worms, methylmercury treatment depleted cellular NAD+.

    In plain wordsIn worms, methylmercury reduced natural NAD+ levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCellular NAD depletion
    Study

    Caenorhabditis elegansn: not reported in source

    methylmercury-exposed worms
    Outcome group
    Mitochondrial function · Whole body

    Source sentences

    Summary
    Worms treated with MeHg showed depletion in cellular NAD( + )levels

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone2

In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  1. 07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In worms unable to synthesize NAD+ from nicotinamide, sensitivity to methylmercury lethality increased versus wildtype worms.

    In plain wordsIn mutant worms unable to produce NAD+ from nicotinamide, methylmercury caused greater lethal sensitivity than in wildtype worms.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseMethylmercury lethality sensitivity
    Study

    Caenorhabditis elegansn: not reported in source

    mutant worms unable to synthesize NAD+ from nicotinamide, exposed to methylmercury
    Comparator
    Wildtype worms
    Outcome group
    Mortality · Whole body

    Source sentences

    Summary
    In a mutant worm line that cannot synthesize NAD( + )from nicotinamide, MeHg lethality and DAergic behavioral deficits were more sensitive to MeHg than wildtype worms, demonstrating the importance of NAD( + )in MeHg toxicity.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  2. 08AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In worms unable to synthesize NAD+ from nicotinamide, methylmercury-induced dopaminergic behavioral deficits were more sensitive than in wildtype worms.

    In plain wordsIn mutant worms unable to produce NAD+ from nicotinamide, behavioral deficits were more sensitive to methylmercury than in wildtype worms.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseMethylmercury behavioral sensitivity
    Study

    Caenorhabditis elegansn: not reported in source

    mutant worms unable to synthesize NAD+ from nicotinamide, exposed to methylmercury
    Comparator
    Wildtype worms
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    In a mutant worm line that cannot synthesize NAD( + )from nicotinamide, MeHg lethality and DAergic behavioral deficits were more sensitive to MeHg than wildtype worms, demonstrating the importance of NAD( + )in MeHg toxicity.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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