Investigation of the Genotoxic Potential of the Marine Toxin C17-SAMT Using the In Vivo Comet and Micronucleus Assays

The contaminant responsible for the atypical toxicity reported in mussels from Bizerte Lagoon (Northern Tunisia) during the last decade has been characterized as C17-sphinganine analog mycotoxin (C17-SAMT). This neurotoxin showed common mouse toxic symptoms, including flaccid paralysis and severe dy...

Full description

Saved in:
Bibliographic Details
Published in:Marine drugs 2022-10, Vol.20 (10), p.619
Main Authors: Marzougui, Zeineb, Huet, Sylvie, Blier, Anne-Louise, Hégarat, Ludovic Le, Tounsi-Kettiti, Haïfa, Kharrat, Riadh, Marrouchi, Riadh, Fessard, Valérie
Format: Article
Language:English
Subjects:
Bioassays
Biocompatibility
Bone marrow
C17-SAMT
Chromosomes
comet assay
Contaminants
Cytoplasm
Damage detection
Deoxyribonucleic acid
DNA
DNA damage
Duodenum
Dyspnea
Food contamination & poisoning
Fungi
Genomes
Genotoxicity
Hazard assessment
Health hazards
Hepatocytes
Lagoons
Life Sciences
Liver
marine biotoxins
Micronuclei
micronucleus assay
Mitosis
Mollusks
Mussels
Mycotoxins
Neurotoxins
Oral administration
Oxidation
Paralysis
Respiration
Seafood
Shellfish
Small intestine
Sphinganine
Spleen
Symptoms
Toxicity
Toxicology
Toxins
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The contaminant responsible for the atypical toxicity reported in mussels from Bizerte Lagoon (Northern Tunisia) during the last decade has been characterized as C17-sphinganine analog mycotoxin (C17-SAMT). This neurotoxin showed common mouse toxic symptoms, including flaccid paralysis and severe dyspnea, followed by rapid death. For hazard assessment on human health, in this work we aimed to evaluate the in vivo genotoxic effects of this marine biotoxin using the classical alkaline and modified Fpg comet assays performed to detect DNA breaks and alkali-labile sites as well as oxidized bases. The micronucleus assay was used on bone marrow to detect chromosome and genome damage. C17-SAMT induces a statistically insignificant increase in DNA tail intensity at all doses in the duodenum, and in the spleen contrary to the liver, the percentage of tail DNA increased significantly at the mid dose of 300 µg/kg b.w/d. C17-SAMT did not affect the number of micronuclei in the bone marrow. Microscopic observations of the liver showed an increase in the number of mitosis and hepatocytes’ cytoplasm clarification. At this level of study, we confirm that C17-SAMT induced DNA damage in the liver but there was no evidence of effects causing DNA oxidation or chromosome and genome damage.
ISSN:1660-3397
1660-3397
DOI:10.3390/md20100619