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Subchronic exposure to fenpyroximate causes multiorgan toxicity in Wistar rats by disrupting lipid profile, inducing

Imen Ayed-Boussema^1,2, Karima Rjiba^1,2, Asma M'nassri^1,2

¹Laboratory of Research on Biologically Compatible Compounds, LR01SE17, University of Monastir, Faculty of Dental Medicine, Monastir, Tunisia.

Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals

|February 1, 2024

Abstract

Background:

Fenpyroximate (FEN) is an acaricide that inhibits the complex I of the mitochondrial respiratory chain in mites. Data concerning mammalian toxicity of this acaricide are limited; thus the aim of this work was to explore FEN toxicity on Wistar rats, particularly on cardiac, pulmonary, and splenic tissues and in bone marrow cells.

Methods:

rats were treated orally with FEN at 1, 2, 4, and 8 mg/Kg bw for 28 days. After treatment, we analyzed lipid profile, oxidative stress and DNA damage in rat tissues.

Results:

FEN exposure increased creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH) activities, elevated total cholesterol (T-CHOL), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) concentrations, while decreasing high-density lipoprotein cholesterol (HDL-C). It inhibited acetylcholinesterase (AChE) activity, enhanced lipid peroxidation, protein oxidation, and modulated antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase). Comet assay indicated that FEN induced a dose-dependent DNA damage, contrasting with the micronucleus test showing no micronuclei formation. Nonetheless, FEN exhibited cytotoxicity to bone marrow cells, as evidenced by a reduction in the number of immature erythrocytes among total cells.

Conclusion:

FEN appears to carry out its genotoxic and cytotoxic activities most likely through an indirect pathway that involves oxidative stress.

Insights

Fenpyroximate (FEN) exposure in rats caused significant oxidative stress, DNA damage, and cytotoxicity, particularly in bone marrow cells. These findings highlight potential mammalian toxicity concerns for this widely used acaricide.

Area of Science:

Toxicology
Environmental Science
Biochemistry

Background:

Fenpyroximate (FEN) is an acaricide targeting mitochondrial complex I in mites.
Limited data exist on the mammalian toxicity of FEN.
This study investigated FEN's effects on Wistar rats, focusing on cardiac, pulmonary, splenic tissues, and bone marrow.

Purpose of the Study:

To evaluate the toxicological effects of Fenpyroximate (FEN) in Wistar rats.
To assess FEN's impact on lipid profiles, oxidative stress, and DNA damage.
To examine FEN's cytotoxicity in bone marrow cells.

Main Methods:

Wistar rats were orally administered FEN (1-8 mg/Kg bw) for 28 days.
Analysis included lipid profiles, oxidative stress markers, and DNA damage assays (Comet assay, micronucleus test).
Cytotoxicity was assessed by examining bone marrow cell populations.

Main Results:

FEN increased cardiac enzymes (CPK, LDH) and altered lipid profiles (elevated T-CHOL, TG, LDL-C; decreased HDL-C).
It inhibited acetylcholinesterase (AChE), induced lipid peroxidation and protein oxidation, and modulated antioxidant enzyme activities.
FEN caused dose-dependent DNA damage (Comet assay) and bone marrow cytotoxicity, evidenced by reduced immature erythrocytes.

Conclusions:

Fenpyroximate (FEN) exhibits significant genotoxic and cytotoxic effects in rats.
Oxidative stress appears to be the primary mechanism underlying FEN's toxicity.
Findings suggest potential mammalian health risks associated with FEN exposure.

Read full analysis

Keywords:

AChE activity Fenpyroximate Wistar rats biochemical markers bone marrow cells genotoxicity heart lungs oxidative stress spleen

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