ArticleJournal of toxicologic pathology2020
Minocycline protects against acrylamide-induced neurotoxicity and testicular damage in Sprague-Dawley rats.
Article in Journal of toxicologic pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Lycopene ameliorates acrylamide-induced reproductive toxicity through enhancement in testicular antioxidant status and upregulation of androgen receptor expression in male Wistar rats.BMC pharmacology & toxicology · 2026Article
- Neuroprotective potential of eugenol against acrylamide-induced brain toxicity by regulating Nrf2/NQO1/HO-1 and NLRP3/NF-κB/IL-1β signaling cascades.Scientific reports · 2026Article
- Identification of differentially expressed genes associated with ferroptosis in ulcerative colitis.PloS one · 2025Article
- Eruca sativa seed extract modulates oxidative stress and apoptosis and up-regulates the expression of Bcl-2 and Bax genes in acrylamide-induced testicular dysfunction in rats.Environmental science and pollution research international · 2021Article
- Effects of Acrylamide-Induced Vasorelaxation and Neuromuscular Blockage: A Rodent Study.Toxics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the protective effects of minocycline against acrylamide (ACR)-induced neurotoxicity and testicular damage in Sprague-Dawley rats. Forty rats were divided into five groups (eight rats each). Group I received saline (0.5 mL/rat) daily for 10 days and served as the untreated control group. Group II received ACR (30 mg/kg body weight (b.w.)) daily for 10 days. Group III received ACR (30 mg/kg b.w.) daily for 10 days and subsequently minocycline (60 mg/kg b.w.) for five days. Group IV received ACR (30 mg/kg b.w.) daily for 10 days followed by saline for five days and served as the control group for the ACR-minocycline-treated group. Group V received minocycline (60 mg/kg b.w.) for five days. All treatments were administered orally. Rats in group I and V showed normal locomotor behavior and normal histology of the brain and testes. Administration of ACR (Group II and IV) resulted in weight loss and gait abnormalities. Furthermore, neuronal degeneration in the hippocampus and cerebellum and degeneration of the seminiferous tubular epithelium with formation of spermatid giant cells were observed. Ultrastructurally, ACR specifically damaged spermatogonia and spermatocytes. Acrylamide was also seen to cause a significant increase of malondialdehyde levels in the brain and testes. Treatment of ACR-administered rats with minocycline (Group III) significantly alleviated the loss of body weight and improved locomotor function. Minocycline also ameliorated neuronal degeneration and seminiferous tubular damage and decreased malondialdehyde concentrations. In conclusion, minocycline protects against neurotoxic effects of acrylamide and seminiferous tubular damage. Decreasing lipid peroxidation by minocycline might play a role in such protection.
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