Protective Effects of Astaxanthin Against Cypermethrin-Induced Neurotoxicity in Rats: Physiological and Histopathological Assessments

Cypermethrin (CYP) is a type II pyrethroid insecticide whose neurotoxicity is closely linked to oxidative stress. Astaxanthin (AST) is a blood–brain barrier-permeable carotenoid with potent antioxidant activity. The present study evaluated the protective effect of two doses of AST against CYP-induced neurotoxicity in rats. Twenty-four adult male rats were divided into four equal groups (n = 6): control (normal saline), CYP (5 mg/kg), CYP + AST (25 mg/kg), and CYP + AST (75 mg/kg), all given orally for 30 days. Brain malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), acetylcholinesterase (AChE), and histopathology were assessed. CYP increased brain MDA by 110.6% (347.85 vs 165.14 nmol/g tissue) and decreased SOD by 38.4%, CAT by 65.2%, GSH by 53.6%, and AChE activity by 51.9% (45.3 vs 94.2 U/g tissue) compared with the control (P < 0.05). Histologically, CYP produced vascular congestion and neuronal degeneration. Both AST doses reduced MDA by about 50% relative to CYP and restored CAT and GSH to levels not significantly different from the control. SOD and AChE showed a dose-related response: the higher dose restored both to control levels (SOD 12.4 U/mg protein; AChE 97.2 U/g tissue), whereas the lower dose produced partial recovery (AChE 68.7 U/g tissue). Unlike the biochemical markers used in the experiment, the histological impact has been not of a dose-dependent nature: at a dose of 25 mg/kg AST, brain lesions were reduced to mild swelling and edema, but with a dose of 75 mg/kg perivascular cuffing and swelling was still observed, which was an inflammation-related type of lesion that was qualitatively more advanced than that at the lower dosage of AST. The use of AST resulted in a decrease in the oxidative damage and cholinergic impairment caused by cypermethrin, especially at the higher dose of AST, whereas the healing of biochemical indicators was aggravated by the fact that no healing was observed in histological portraits, which is one of the remarkable findings of the study.

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Journal
Journal of Agriculture Aquaculture and Animal Science
Published
2026-11-01
DOI
https://doi.org/10.69739/jaaas.v3i2.2522
Primary Topic
Pesticide Exposure and Toxicity
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article
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article

Protective Effects of Astaxanthin Against Cypermethrin-Induced Neurotoxicity in Rats: Physiological and Histopathological Assessments

Hawraa M. Murad, Ghusoon Abdul Kareem Neamah, Ahmed Neema AL-Mussawy
1 links
Journal of Agriculture Aquaculture and Animal Science
Pesticide Exposure and Toxicity
article

Protective Effects of Astaxanthin Against Cypermethrin-Induced Neurotoxicity in Rats: Physiological and Histopathological Assessments

Hawraa M. Murad, Ghusoon Abdul Kareem Neamah, Ahmed Neema AL-Mussawy
article en

Abstract

Cypermethrin (CYP) is a type II pyrethroid insecticide whose neurotoxicity is closely linked to oxidative stress. Astaxanthin (AST) is a blood–brain barrier-permeable carotenoid with potent antioxidant activity. The present study evaluated the protective effect of two doses of AST against CYP-induced neurotoxicity in rats. Twenty-four adult male rats were divided into four equal groups (n = 6): control (normal saline), CYP (5 mg/kg), CYP + AST (25 mg/kg), and CYP + AST (75 mg/kg), all given orally for 30 days. Brain malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), acetylcholinesterase (AChE), and histopathology were assessed. CYP increased brain MDA by 110.6% (347.85 vs 165.14 nmol/g tissue) and decreased SOD by 38.4%, CAT by 65.2%, GSH by 53.6%, and AChE activity by 51.9% (45.3 vs 94.2 U/g tissue) compared with the control (P < 0.05). Histologically, CYP produced vascular congestion and neuronal degeneration. Both AST doses reduced MDA by about 50% relative to CYP and restored CAT and GSH to levels not significantly different from the control. SOD and AChE showed a dose-related response: the higher dose restored both to control levels (SOD 12.4 U/mg protein; AChE 97.2 U/g tissue), whereas the lower dose produced partial recovery (AChE 68.7 U/g tissue). Unlike the biochemical markers used in the experiment, the histological impact has been not of a dose-dependent nature: at a dose of 25 mg/kg AST, brain lesions were reduced to mild swelling and edema, but with a dose of 75 mg/kg perivascular cuffing and swelling was still observed, which was an inflammation-related type of lesion that was qualitatively more advanced than that at the lower dosage of AST. The use of AST resulted in a decrease in the oxidative damage and cholinergic impairment caused by cypermethrin, especially at the higher dose of AST, whereas the healing of biochemical indicators was aggravated by the fact that no healing was observed in histological portraits, which is one of the remarkable findings of the study.

Journal of Agriculture Aquaculture and Animal ScienceVol. 3(2)
University of Kerbala (IQ), Al-Qasim Green University (IQ)
Good health and well-being
Openalex Percentile: Top 15%
Pesticide Exposure and Toxicity
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