Related Experiment Video
Updated: Jun 12, 2026
12:03
Viability Assays for Cells in Culture
Published on: January 20, 2014
Toxicology studies with N-acetyl-L-serine
E L M van de Mortel1, Z A Shen, J F Barnett
1Pioneer Hi-Bred International Inc, Ankeny, IA, United States.
Summary
N-Acetyl-L-serine (NAS) is safe, showing no mutagenicity or genotoxicity in toxicology studies. Acute and repeated dose studies in rats found no adverse effects, establishing a high no-observed-adverse-effect-level (NOAEL).
Area of Science:
- Toxicology
- Nutritional Biochemistry
- Food Safety
Background:
- N-Acetyl-L-serine (NAS) is a naturally occurring amino acid derivative found in dietary proteins and foods.
- Understanding the safety profile of NAS is crucial given its presence in the human diet.
Purpose of the Study:
- To comprehensively evaluate the toxicological safety of N-Acetyl-L-serine (NAS).
- To assess the potential for mutagenicity, genotoxicity, acute toxicity, and systemic toxicity following repeated exposure.
Main Methods:
- Reverse bacterial mutation assay (Ames test) for mutagenicity.
- In vivo bone marrow micronucleus assay in mice for genotoxicity.
- Acute oral toxicity study in Sprague-Dawley (SD) rats (2000 mg/kg).
- 28-day repeated dose dietary toxicity study in SD rats (100, 500, 1000 mg/kg/day).
Main Results:
- NAS demonstrated no mutagenic or genotoxic potential in bacterial and mouse assays.
- No mortality or adverse effects were observed in acute oral toxicity studies.
- Repeated dose studies revealed no adverse effects, with no-observed-adverse-effect-levels (NOAELs) of 839.7 mg/kg/day (males) and 893.6 mg/kg/day (females).
Conclusions:
- N-Acetyl-L-serine (NAS) is not mutagenic or genotoxic.
- NAS exhibits a low acute toxicity profile.
- The established NOAELs indicate a wide safety margin for dietary exposure to NAS.
More Related Videos
Related Concept Videos
01:23Toxicity 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...
01:26Toxic Reactions: Overview
When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
01:17Antidotes
Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
01:24Drug 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...
01:00Drug 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...
01:24Phase II Reactions: Acetylation Reactions
Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...