Prenatal double-hit with aluminium and cadmium mediate testicular atrophy and hypothalamic hypoplasia: the role of oxido-nitrergic stress and endocrine perturbations.

There is limited experimental evidence on the biochemical consequences of aluminium (Al) and cadmium (Cd) co-exposures during pregnancy and postnatal life.This study investigated the impacts of perinatal Al chloride (AlCl3) and Cd chloride (CdCl2) co-exposures on neuroendocrine functions in mice offspring during postnatal life. The study comprised of four pregnant experimental groups. Group 1 received AlCl3 (10 mg/kg), group 2 were administered CdCl2 (1.5 mg/kg), while group 3 received both AlCl3 (10 mg/kg) and CdCl2 (1.5 mg/kg) (AlCl3+CdCl2), and group 4 received saline (10 mL/kg) only and served as control group. All experimental animals were chemically exposed once daily from gestation days 7-20. Upon delivery, male pups were regrouped based on maternal chemical exposure on postnatal day 21 (PND 21) and allowed to grow to adulthood until PND 78, after which they were sacrificed for assessment of neuroendocrine markers and histological investigations. There was no statistical significance (p > 0.05) on follicle stimulating hormone, testosterone, estrogen and progesterone, thyroid stimulating hormone, thyroxine (T4) in all treatment groups relative to controls|. However, AlCl3 and AlCl3-CdCl2 significantly (p < 0.05) reduced triiodothyronine (T3) levels, with a profound increase in T3:T4 ratio by AlCl3, and AlCl3+CdCl2 compared to control. Furthermore, pups from pregnant mice treated with CdCl2 and AlCl3+CdCl2 demonstrated increased testicular malondialdehyde concentration with increased catalase activity relative to controls, suggesting oxidative imbalance. In addition, AlCl3, CdCl2, and AlCl3+CdCl2 exposures induced testicular and hypothalamic architectural disruption compared to controls, with marked architectural derangement in the AlCl3+CdCl2 group. Our findings suggest that prenatal co-exposures to Alcl3 and CdCl2 induce testicular and hypothalamic alterations in offspring via a testicular oxidative stress and thyrotoxicosis-dependent mechanisms.

Datura metel stramonium exacerbates behavioral deficits, medial prefrontal cortex, and hippocampal neurotoxicity in mice via redox imbalance.

BACKGROUND: Datura metel (DM) stramonium is a medicinal plant often abused by Nigerians due to its psychostimulatory properties. Hallucinations, confusion, agitation, aggressiveness, anxiety, and restlessness are reported amongst DM users. Earlier studies suggest that DM induces neurotoxicity and affect brain physiology. However, the exact neurological effects of DM extract in the medial prefrontal cortex (mPFC) and hippocampal morphology have not been elucidated. In this study, we evaluated the hypothesis that oral exposure to DM extract exerts a neurotoxic effect by increasing oxidative stress in the mPFC and the hippocampus and induces behavioral deficits in mice. RESULTS: DM methanolic extract exposure significantly increased MDA and NO levels and reduced SOD, GSH, GPx and CAT activities in mice brains. In addition, our results showed that DM exposure produced cognitive deficits, anxiety, and depressive-like behaviour in mice following oral exposure for 28 days. Moreover, the mPFC and hippocampus showed neurodegenerative features, loss of dendritic and axonal arborization, a dose-dependent decrease in neuronal cell bodies' length, width, area, and perimeter, and a dose-dependent increase in the distance between neuronal cell bodies. CONCLUSIONS: Oral exposure to DM in mice induces behavioural deficits, mPFC and hippocampal neuronal degenerations via redox imbalance in the brain of mice. These observations confirm the neurotoxicity of DM extracts and raises concerns on the safety and potential adverse effects of DM in humans.

Antioxidative properties of Ocimum gratissimum alters Lead acetate induced oxidative damage in lymphoid tissues and hematological parameters of adult Wistar rats.

Lead exposure is a well-known environmental hazard. Its accumulation in humans may pose a danger to health. The present study investigated the beneficial effect of Ocimum gratissimum extract (OG) in reducing lead acetate (LA) induced oxidative damage in the spleen, thymus, and hematological indices. We employed an in vivo model of LA induced Wistar rats and administered 125 mg/kg/bw and 250 mg/kg/bw of OG extracts respectively. Our control groups were divided into 2; the first group received normal saline, feed, and water while the second group was administered OG extracts only. We assessed the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the thymus and spleen and estimated percentages of blood cells. Our results showed that LA induces oxidative damage by significantly elevating MDA and diminishing GSH levels, SOD, and CAT activities. LA administration led to a significant decline in blood parameters. However, co-administration with OG compensated oxidative stress by significantly reducing MDA, increasing GSH, SOD, and CAT. Oral administration of OG to rats attenuated anemia, thrombocytopenia, leucocytosis, eosinophilia, monocytosis, and neutropenia induced by LA. The present study indicates that LA induced Spleen, thymus, and blood toxicity, which was reversed by oral OG administration.