Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Vitamins

Vitamins

Vitamins, derived from the Latin word for life, are essential organic substances required in small quantities for optimal growth and overall well-being. Unlike other organic nutrients, vitamins don't act as sources of energy or building materials but rather facilitate these nutrients' utilization by the body. Vitamins are predominantly coenzymes, assisting enzymes in specific chemical actions, like the oxidation of glucose for energy involving B vitamins. Most vitamins are not produced in our...

Toxicity Testing in Animals

Toxicity Testing in Animals

Toxicity tests in animals are grounded on two main assumptions: first, the effects observed in laboratory animals can be extrapolated to humans, especially when adjusted for body surface area; second, high-dose exposure in animals is essential to identify potential human hazards from lower doses. This is based on the quantal dose-response concept, which faces the challenge of extrapolating results from relatively few test animals to much larger human populations. For example, a 0.01% incidence...

Drug Toxicity: Overview

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...

Drug Toxicity: Dose-Dependent Reactions

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

Bioactivation and Tissue Toxicity

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...

Drugs Affecting Neurotransmitter Synthesis

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Undiagnosed Diabetes and Prediabetes in Yemen: A Growing Public Health Crisis in the Shadow of Conflict.

Medicina (Kaunas, Lithuania)·2026

Same author

Effectiveness of Tocotrienol-Rich Fraction in Older Adults: Protocol for a Randomized, Double-Blind, Placebo-Controlled Trial.

JMIR research protocols·2025

Same author

CRISPR/Cas9 mediated ENT2 gene knockout altered purine catabolic pathway and induced apoptosis in colorectal cell lines.

PloS one·2025

Same author

Shifting Perspectives on the Role of Tocotrienol vs. Tocopherol in Brain Health: A Scoping Review.

International journal of molecular sciences·2025

Same author

Hydroxychavicol in Combination with 5-Fluorouracil Induced Apoptosis by Inhibiting Purine Metabolism in HT-29 and DLD-1 Cell Lines.

Chinese journal of integrative medicine·2025

Same author

Evaluating the Role of Vitamin D in Prediabetes Management, Insights from RCTs in the MENA Region: A Comprehensive Systematic Review.

Journal of clinical medicine·2025

Search research articles

Related Experiment Video

Updated: Jun 26, 2026

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

Published on: May 5, 2009

Is vitamin E toxic to neuron cells?

Sue Mian Then¹, Musalmah Mazlan, Gapor Mat Top

¹UKM Medical Molecular Biology Institute (UMBI), Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Universiti Kebangsaan Malaysia, 7th Floor Clinical Block, Jalan Yaacob Latiff, Bandar Tun Razak, Cheras, Kuala Lumpur, Malaysia. suemian@mail.hukm.ukm.my

Cellular and Molecular Neurobiology

|January 28, 2009

Summary

Both alpha-tocopherol (alphaT) and gamma-tocotrienol (gammaT3) protect neurons from H(2)O(2)-induced apoptosis. However, gammaT3 exhibits a stronger pro-apoptotic tendency than alphaT by activating specific molecular pathways without H(2)O(2).

More Related Videos

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Published on: June 9, 2017

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Published on: February 5, 2015

Related Experiment Videos

Last Updated: Jun 26, 2026

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

Published on: May 5, 2009

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Published on: June 9, 2017

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Published on: February 5, 2015

Area of Science:

Neuroscience
Biochemistry
Cell Biology

Background:

Tocopherols and tocotrienols possess non-antioxidant properties, including alpha-tocopherol's role in the PKC pathway and gamma-tocotrienol's anti-cancer effects.
Understanding the dual roles of these compounds in neuronal apoptosis is crucial for therapeutic development.

Purpose of the Study:

To investigate the anti-apoptotic or pro-apoptotic effects of alpha-tocopherol (alphaT) and gamma-tocotrienol (gammaT3) in hydrogen peroxide (H(2)O(2))-induced neuronal apoptosis.
To compare the neuroprotective and neurotoxic profiles of alphaT and gammaT3 in primary cerebellar neuron cultures.

Main Methods:

Primary cerebellar neuron cultures were treated with H(2)O(2) to induce apoptosis, with or without pre-treatment of alphaT or gammaT3.
Cellular uptake, neurotoxicity, and expression of apoptosis-related proteins (Bax, Bcl-2, p53) and signaling molecules (p38 MAPK) were analyzed.
The Bcl-2/Bax ratio was used as a survival index.

Main Results:

Low concentrations (< or =10 microM) of alphaT and gammaT3 attenuated H(2)O(2)-induced apoptosis, while high concentrations (> or =100 microM) of gammaT3 were neurotoxic.
Both alphaT and gammaT3 increased Bax and Bcl-2 expression, enhancing the Bcl-2/Bax survival index in H(2)O(2)-treated neurons.
GammaT3 alone decreased the Bcl-2/Bax ratio, decreased p53 expression, and activated p38 MAPK phosphorylation, indicating a pro-apoptotic tendency, unlike alphaT.

Conclusions:

Low-dose alphaT and gammaT3 provide neuroprotection against H(2)O(2) via antioxidant mechanisms.
GammaT3 exhibits a stronger pro-apoptotic tendency than alphaT by activating apoptotic pathway molecules independently of H(2)O(2).
Differential effects of tocopherols and tocotrienols highlight the complexity of their roles in neuronal cell fate.