An in vivo and in silico probing of the protective potential of betaine against sodium fluoride-induced neurotoxicity.

Excessive fluoride exposure beyond the tolerable limit may adversely impacts brain functionality. Betaine (BET), a trimethyl glycine, possesses antioxidant, anti-inflammatory and anti-apoptotic functions, although the underlying mechanisms of the role of BET on fluoride-induced neurotoxicity remain unelucidated. To assess the mechanism involved in the neuro-restorative role of BET on behavioural, neurochemical, and histological changes, we employed a rat model of sodium fluoride (NaF) exposure.

Prepubertal Repeated Berberine Supplementation Enhances Cerebrocerebellar Functions by Modulating Neurochemical and Behavioural Changes in Wistar Rats.

Antioxidant-rich supplementation plays an essential role in the function of mammals' central nervous system. However, no research has documented the effect of berberine (BER) supplementation on the cerebrocerebellar function of prepubertal rats. The present study was designed to investigate the impact of BER supplementation on neurochemical and behavioural changes in prepubertal male rats.

Modulation of the Nrf-2 and HO-1 signalling axis is associated with Betaine's abatement of fluoride-induced hepatorenal toxicities in rats.

Sodium fluoride (NaF) ingestion has several detrimental effects in humans and rodents. NaF mechanisms of toxicity include perturbation of intracellular redox homeostasis and apoptosis. Betaine (BET) is a modified amino acid with anti-inflammatory, antioxidant, and anti-apoptotic properties.

3-Indolepropionic acid mitigates sub-acute toxicity in the cardiomyocytes of epirubicin-treated female rats.

Epirubicin (EPI) is an effective chemotherapeutic against breast cancer, though EPI-related cardiotoxicity limits its usage. Endogenously derived 3-indolepropionic acid (3-IPA) from tryptophan metabolism is of interest due to its antioxidant capabilities which may have cardioprotective effects. Supplementation with 3-IPA may abate EPI's cardiotoxicity, and herein we studied the possibility of lessening EPI-induced cardiotoxicity in Wistar rats.

Exposure to lead and dietary furan intake aggravates hypothalamus-pituitary-testicular axis toxicity in chronic experimental rats.

Lead (Pb) and furan are toxic agents, and persistent exposure may impair human and animal reproductive function. We therefore explored the effects of Pb and furan on male rat hypothalamic-pituitary-gonadal reproductive status, oxidative stress, inflammation, and genomic integrity. We found that co-exposure to Pb and furan reduced the activities of testicular function enzymes, endogenous antioxidant levels, total sulfhydryl group, and glutathione.

Co-exposure to aflatoxin B1 and therapeutic coartem worsens hepatic and renal function through enhanced oxido-inflammatory responses and apoptosis in rats.

Aflatoxin B1 (AFB) is a mycotoxin synthesised as a secondary metabolite by members of the Aspergillus species contaminating agricultural produce. Aspergillus species thrive in tropical climes, endemic to malaria. Artemisinin-based combination therapies (ACTs) effectively treat and prevent malaria recrudescence; Coartem (COA) is an ACT whose toxicity is evident.

A biochemical and histology experimental approach to investigate the adverse effect of chronic lead acetate and dietary furan on rat lungs.

Despite lead widespread environmental pollution, its effect on humans and livestock's respiratory systems remains inadequately investigated. Similarly, furan is industrially relevant with enormous environmental presence. Lead and furan can be ingested -via lead pipes contaminated water and heat-treated food respectively.

Influence of furan and lead co-exposure at environmentally relevant concentrations on neurobehavioral performance, redox-regulatory system and apoptotic responses in rats.

Furan and lead are contaminants of global concern due to the potential public health threat associated with their exposure. Herein, the neurobehavioral performance, biochemical effects and histological alterations associated with co-exposure to furan (8 mg/kg) and lead acetate at low, environmentally realistic concentrations (1, 10 and 100 µg PbAc/L) for 28 uninterrupted days were investigated in rats. The results demonstrated that locomotor, motor and exploratory deficits associated with separate exposure to furan and lead was exacerbated in the co-exposed rats.

Apigeninidin-enriched (L. Moench) extracts alleviate Aflatoxin B-induced dysregulation of male rat hypothalamic-reproductive axis.

We examined the protective effect of the apigeninidin (API)-enriched fraction from sheaths extracts (SBE-05, SBE-06, and SBE-07) against aflatoxin B (AFB)-induced dysregulation of male rat's reproductive system that may trigger infertility. Male rats (160 ± 12 g) were treated with AFB (50 µg/kg) along with 5 or 10 mg/kg of SBE-05, SBE-06, and SBE-07 for 28 days. Subsequently, we assessed the reproductive hormone-prolactin, FSH, LH, testosterone levels, and testicular function enzymes.

3-Indolepropionic acid prevented chlorpyrifos-induced hepatorenal toxicities in rats by improving anti-inflammatory, antioxidant, and pro-apoptotic responses and abating DNA damage.

The application of chlorpyrifos (CPF), an organophosphorus pesticide to control insects, is associated with oxidative stress and reduced quality of life in humans and animals. Indole-3-propionic acid (IPA) is a by-product of tryptophan metabolism with high antioxidant capacity and has the potential to curb CPF-mediated toxicities in the hepatorenal system of rats. It is against this background that we explored the subacute exposure of CPF and the effect of IPA in the liver and kidney of thirty rats using five cohort experimental designs (n = 6) consisting of control (corn oil 2 mL/kg body weight), CPF alone (5 mg/kg), IPA alone (50 mg/kg), CPF + IPA (5 mg/kg + 25 mg/kg), and CPF + IPA (5 mg/kg + 50 mg/kg).

3-Indolepropionic acid upturned male reproductive function by reducing oxido-inflammatory responses and apoptosis along the hypothalamic-pituitary-gonadal axis of adult rats exposed to chlorpyrifos.

We examined the effect of 3-Indolepropionic acid (3-IPA), an antioxidant on the organophosphorus pesticide chlorpyrifos (CPF)-induced reproductive toxicity in rats. The five experimental rat cohorts were treated per os for 14 consecutive days as follows: Control (Corn oil 2 mL/kg body weight), CPF alone (5 mg/kg), 3-IPA alone (40 mg/kg) and the co-treated rat cohorts (CPF:5 mg/kg + 3-IPA: 20 or 40 mg/kg). Biomarkers of testicular and epididymal function, oxidative stress, myeloperoxidase (MPO) activity and the levels of nitric oxide (NO), reactive oxygen and nitrogen (RONS) species and lipid peroxidation (LPO) were assessed.

Decrease in reproductive dysfunction using aflatoxin B1 exposure: a treatment with 3-indolepropionic acid in albino Wistar rat.

We assessed the individual and combined consequence of 3-indolepropionic acid on aflatoxin B1-induced reproductive toxicity in rats. The experimental cohorts were dosed for four consecutive weeks with aflatoxin B1 (50 μg/kg), 3-indolepropionic acid (50 mg/kg), and both (aflatoxin B1: 50 μg/kg + 3-indolepropionic acid: 25 or 50 mg/kg), and the untreated control. Following sacrifice, biomarkers of testicular, epididymal and hypothalamic oxidative status, lipid peroxidation, reactive oxygen and nitrogen species, nitric oxide levels and myeloperoxidase activity were determined.