2022 Citations

Mentha longifolia L (ML) is locally used as an herbal contraceptive. We aim to assess the toxicity profile and validate the antifertility effects of its leaves in male rats. Adult male Sprague Dawley rats (n = 10 animals/group) were divided into four groups. The Control group received .9% saline, while groups II, III, and IV received 50, 75, and 100 mg/kg/day ML doses for 28 days. ML induced a dose-dependent decrease in percent fertility as well as the number of pups born in ML preexposed pairs, with maximum change observed in the ML3 group (60%, 3.75 ± 1.25) as compared to control (100%, 8.75 ± .48) group. A significant (P < .01) decrease in the rate of daily sperm production was observed in the ML3 group (.86 ± .16) in contrast to the control (2.93 ± .05). The levels of catalase and superoxide dismutase declined significantly in treatment groups (ML1-P < .001, ML2-P < .05, and ML3-P < .01). A significant increase in the production of reactive oxygen species (P < .001) was

Maternal separation (MS) is a key contributor to neurodevelopmental disorders, including learning disabilities. To test the hypothesis that dopamine signaling is a major factor in this, an atypical new dopamine transporter (DAT) inhibitor, CE-123, was assessed for its potential to counteract the MS-induced spatial learning and memory deficit in male and female rats. Hence, neonatal rats (postnatal day (PND)1 to 21) were exposed to MS (180 min/day). Next, the acquisition of spatial learning and memory (Barnes maze task) and the expression of dopamine D1 receptor, dopamine transporter (DAT), and the neuronal GTPase, RIT2, which binds DAT in the vehicle-treated rats were evaluated in the prefrontal cortex and hippocampus in the adolescent animals. The results show that MS impairs the acquisition of spatial learning and memory in rats, with a more severe effect in females. Moreover, the MS induced upregulation of DAT and dopamine D1 receptors expression in the prefrontal cortex and hippocampus in adolescent rats.

Although long-term smoking has been associated with chronic kidney disease, its effect on kidney function in early stages has not been clarified. Therefore, the proposed objectives were: (1) to identify subclinical kidney damage in smokers, through a panel of biomarkers; (2) to evaluate the progression of subclinical kidney damage after two years of consumption in these patients; and (3) study whether quitting smoking reduces kidney damage. A prospective study was carried out (patients recruited from a primary care centre and a clinical smoking unit). Kidney function was assessed using a panel of biomarkers and compared between smokers and non-smokers, taking into account potential risk factors for kidney damage. These results show, for the first time in the literature, the relationship between smoking and early (subclinical) kidney damage and provide a panel of biomarkers capable of detecting this condition (Neutrophil gelatinase-associated lipocalin, Kidney injury molecule-1, N-acetyl-beta-D-glucosaminidase

The present study aims to assess the effect of a heavy metal burden on general health, biochemical parameters, an antioxidant enzyme, and reproductive hormone parameters in adult male brick kiln workers from Pakistan. The study participants (n = 546) provided demographic data including general health as well as body mass index. Blood was collected to quantitatively assess hematological, biochemical, and reproductive hormone parameters as well as heavy metal concentrations using both atomic absorption spectroscopy (AAS) and particle-induced X-ray emission (PIXE). The data showed that 10% of the brick kiln workers were underweight and 10% obese (P = 0.059), with workers also reporting multiple health issues. Heavy metal concentrations utilizing AAS revealed significantly (p = 0.000) higher levels of cadmium, chromium, and nickel, while PIXE detected more than permissible levels of Si, P, S, Cl, K, Ca, Zn, Ti (p = 0.052), Mn (p = 0.017), Fe (p = 0.055), Co (p = 0.011), Ni (p = 0.045), and Cu (p = 0.003), in the

Acetaminophen (APAP)-induced liver injury (AILI) is the most frequent cause of acute liver failure; but the underlying mechanisms still remain obscure. Macrophages and endoplasmic reticulum (ER) stress play an important role in the pathogenesis of AILI. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is a newly identified 18-kDa soluble protein, whose expression and secretion are stimulated by ER stress. To investigate the role of myeloid cell MANF in the pathogenesis of AILI, we assayed serum and liver samples from AILI model mice and patients with drug-induced liver injury (DILI). We demonstrated that the levels of MANF were elevated in patients with DILI and in mice with AILI. Moreover, myeloid-specific MANF knockout mice were generated and used. It was observed that a delayed liver recovery from myeloid-specific MANF gene knockout mice following APAP overdose compared to that from wild-type mice. MANF deficiency in myeloid cells resulted in increased infiltrating monocyte-derived macrophages (M