ArticleBiological trace element research2026
Selenium and Lycopene Ameliorate Methamphetamine-induced Neurotoxicity in Offspring Rats by Suppressing Oxidative Stress, Neuro-inflammation, and Apoptosis.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Methamphetamine (METH) is an illicit drug and sympathetic nervous system stimulant that easily crosses the placenta due to its low molecular weight and high lipid solubility, thus affecting the pregnant mother and fetus. Considering the antioxidant and anti-inflammatory properties of selenium (Se) and lycopene (LYCO), as well as their ability to cross the blood-brain barrier and placental and be secreted into milk, this study aimed to evaluate the combined effects of Se and LYCO on METH-induced neurotoxicity in offspring rats. Thirty pregnant rats were divided into seven groups (n = 3-6), including control, METH (5 mg/kg, ip), METH and Se (2.5 mg/kg, gavage), METH and LYCO (10 mg/kg, gavage), METH in combination of Se with LYCO, Se, and LYCO. METH (3 consecutive days a week), Se (every other day), and LYCO (once daily) were administered for 42 days during pregnancy and breastfeeding. After the end of the study, antioxidant, oxidant, pro-inflammatory, and apoptosis factors were measured. Histological and immunofluorescence examinations with markers glial fibrillary acidic protein (GFAP) and vimentin were performed. Treatment with Se and LYCO reduced the levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), reactive oxygen species (ROS), thiobarbituric acid-reactive substances (TBARS), and the expression of nuclear factor kappa B (NF-κB), Bcl-2-associated x protein (Bax), GFAP, and vimentin proteins and increased the level of total thiol, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and the expression of B-cell lymphoma-2 (Bcl-2) protein compared to the METH group. Treatment with Se and LYCO could modulate METH-induced neurotoxicity in offspring rats by suppressing oxidative stress, neuroinflammation, apoptosis, and the expression of NF-κB, GFAP, and vimentin proteins.
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