The Allium cepa assay represents a crucial in vivo model for evaluating the cytotoxicity and genotoxicity of substances. This study investigated the cytogenotoxicity of mercury chloride (HgCl₂), a laboratory disinfectant and catalyst, using the Allium cepa assay. Mitotic slides were prepared from onion root tip cells grown on media supplemented with different concentrations of HgCl₂ (0%, 0.2%, 0.4%, 0.6%, 0.8%, and 1.0%). The slides were observed to evaluate cytogenotoxicity based on the assessment of the mitotic index, mitotic inhibition, clastogenic effect, and root length. The results showed that the concentrations used are harmful to the cell, leading to adverse impacts on the mitotic index, mitotic inhibition, root growth, and chromosome structure. Different chromosomal aberrations, such as bridge formation, fragmentation fragments, wandering chromosomes, stickiness, binucleate cells, and micronucleus formation, were detected depending on the concentration. Although lower concentrations (0.2–0.4%) had fewer effects on the cells, they still had a significant cytogenotoxic effect (p < 0.05) compared to that of the control (0.0%). The higher the concentration, the greater the effects on clastogenic changes. The abnormalities in both mitotic spread and root growth indicate that mercury chloride is cytotoxic even at low concentrations and can cause mito-depressive effects at higher concentrations. The results of this investigation can be used as a guide to guarantee sufficient safety precautions for people and organs during the regular use of HgCl₂.

Glucocorticoids have therapeutic benefits in the management of several inflammatory and immunological disorders. Despite these medicinal effects, they have the drawback of causing metabolic disorders such as hyperglycemia, insulin resistance etc., which is known to be a key indicator of metabolic syndrome. Metabolic syndrome is a major predisposing factor to type 2 diabetes mellitus and cardiomyopathy. This study was designed to compare and evaluate the effects of saxagliptin, metformin and intranasal insulin (when used singly or in combination) on dexamethasone induced insulin resistance. Fifty-six female rats were randomly assigned into eight groups. Group 1 represented the control; Group 2 was administered with dexamethasone (1mg/kg) (untreated); Group 3 received dexamethasone + intranasal insulin (2IU); Group 4 received dexamethasone + intranasal insulin + metformin (40mg/kg); Group 5; received dexamethasone + intranasal + saxagliptin (8mg/kg); Group 6 received dexamethasone + metformin (40mg/kg); Group 7 received dexamethasone + saxagliptin (8mg/kg); Group 8 received dexamethasone + saxagliptin(8mg/kg) + metformin(40mg/kg). Treatments were given for one week. At the end of the study, blood samples were collected for biochemical assays and pancreas excised for histological examination. Dexamethasone (1mg/kg) induced hyperglycemia, hyperinsulinemia, dyslipidemia, impaired glucose tolerance and disrupted the structural integrity of the pancreas. Treatment with saxagliptin, metformin and their combination significantly decreased blood glucose level, decreased LDL Level and improved glucose tolerance. The selected hypoglycemic agents used in present study ameliorate the dexamethasone induced hyperglycemia and insulin resistance of which the combination of metformin with saxagliptin showed greater efficacy.

Objective. To evaluate the effect of the chronic use of combined oral contraceptives (COCs: ethinyl estradiol and levonorgestrel) on the indices of metabolic syndrome in adult female Wistar rats and possible therapeutic management. Materials and Methods. 64 female Wistar rats received either distilled water, norethindrone (NOR), COC, intranasal insulin (INI), metformin (MET), saxagliptin (SAX), INI+MET, and INI+SAX. After 8 weeks of exposure to COC, the animals were sorted into the therapeutic groups. Several parameters were assayed for, such as body weight changes, fasting blood glucose (FBG) level, insulin levels, inflammatory cytokines, and glycated hemoglobin (Hb1Ac). Results. The levels of FBG, insulin, and Hb1Ac were increased consequent upon COC treatment. Treatment with INI+SAX and INI+MET reduced significantly the levels of FBG and Hb1Ac; in addition, the level of insulin was significantly increased in the INI+MET groups ( ). Serum lipid profile analysis showed a statistical reduction in high-density lipoprotein (HDL) level; this reduction was also significantly reversed in the INI+SAX group. Reduced catalase activity observed in the COC group was reversed in the INI+MET group ( ). A nonsignificant increase in the level of TNF-α as a result of COC treatment was reversed by INI and INI+MET treatment. Liver GLUT4 and G-6-phosphate levels were significantly increased by COC treatment, and this effect was reversed by INI+SAX in both assays, respectively ( ). Conclusions. The use of MET and SAX in combination with INI has been shown to reverse some indices of MetS. This study proposes a clinical phase to backup and ascertain these preclinical findings.

Traditional Tobacco smoking (TTS) is globally known as the single largest avoidable risk factor for a broad range of diseases. It is believed to be a “pandemic” because of its deleterious global impact on public health. Over a century ago, there has been a wide spread of tobacco cigarettes, originating particularly from the Americas; and most recently alternative tobacco products, such as heated tobacco products (HTPs), nicotine pouches, e-cigarettes, etc. This is due to the perceived safety of the latter. Data for this review were gotten through a rigorous search of scientific literatures on PubMed, Elsevier, Google scholar and Scopus. Unbiased findings on these search engines were included in this study, while claims that are unscientific were excluded. The deleterious health effects of e-cigarette aerosols (ECA) have been linked largely to the e-juice or e-liquid which majorly contains nicotine, flavorings, propylene glycol and other unregulated additives. In the respiratory system, TTS and ECA cause increase in pulmonary macrophage count and higher cell influx. However, TTS caused a higher lipid peroxidation judged by an increase in malondialdehyde (MDA) level. ECA caused a shift in the histo-architecture of the lungs, featuring an increase in volume density of the alveolar space which is associated with Chronic Obstructive Pulmonary Disease (COPD). Studies involving the cardiovascular system explored the e-liquid constituents such as nicotine, linked to atherosclerosis; cardiac tissue remodeling and cardiotoxic thermal metabolites of propylene glycol. On cardiac tissue remodeling, ECA caused significant increase in angiogenesis in mouse heart tissues, coupled with increase collagen production but not tissue fibrosis. This suggests that acute exposure to ECA did not adversely affect contractile functions or fibrosis. However, this was contrary with TTS, which showed inhibition of angiogenesis and induction of cardiac fibrosis. The increasing use of ECA amongst young adults showed more tendency for neurological defects when compared with TTS (since its consumption is reduced), this is mainly due to combinatory neurotoxic effects of nicotine, flavorings, formaldehyde, etc., causing a negative effect on cognition and attention span.

Background and Purpose: A Nigerian-formulated polyherbal supplement (PHS) is consumed for its folkloric claims of boosting the immune system. The aim of this study was to toxicologically evaluate a 30-day administration of PHS. Methods: Gas Chromatography/Mass Spectrometry (GC/MS) analysis was carried out on the ethanol extract of PHS. Thirty-two Wistar rats were randomly assigned to four groups. One group served as control while the other three groups were administered 250, 500, and 1000 mg/kg/day of PHS for 30 consecutive days. The animals were anesthetized, and cardiac puncture was used to obtain whole blood for hematology and serum biochemistry. In vivo, antioxidant assays were also carried out on the liver homogenates. The liver, kidneys, and heart were examined histologically. Results: The most abundant compounds identified were eucalyptol, alpha-pinene, and phytol. There were no adverse hematological effects. Total cholesterol, LDL-C, and catalase were reduced significantly (P<0.05). At 1000 mg/kg/day, there was a significant increase in creatinine, sodium ion, and glutathione peroxidase concentration. The histological examination of the heart, kidneys, and liver revealed that PHS did not cause any major tissue lesions at 250 and 500 mg/kg/day. Tissue lesions and pathologies were obvious at 1000 mg/kg/day. Conclusion: The polyherbal supplement seems to be relatively safe if used at doses up to 250 mg/kg/day. Higher doses may cause renal and hepatic lesions.

The objective of this study is to evaluate the effect of the chronic use of combined oral contraceptives (COC; Ethinyl estradiol and Levonorgestrel) on the indices of metabolic syndrome in adult female wistar rats; and possible therapeutic management.  In this study, 64 female wistar rats received either distilled water, Norethindrone (NOR), COC, Intranasal insulin (INI), Metformin (MET), Saxagliptin (SAX), INI+MET and INI+SAX. The mice were divided into therapy groups after 8 weeks of COC exposure. Body weight fluctuations, fasting blood glucose (FBG) levels, insulin levels, inflammatory cytokines, glycated hemoglobin (Hb1Ac), and other indicators were measured. Treatment with INI+SAX and INI+MET, reduced significantly the levels of FBG and Hb1Ac, in addition the level of insulin was significantly increased in the INI+MET groups (p \(\leq\) 0.05). Serum lipid profile analysis revealed a statistically significant decline in HDL levels, which was considerably restored in the INI+SAX group. Reduced catalase activity observed in the COC group was reversed in the INI+MET group (p \(\leq\) 0.05). A non-significant increase in the level of TNF-\(\alpha\) as a result of COC treatment was reversed by INI and INI + MET treatment. The use of MET, SAX, and INI in conjunction has been demonstrated to reverse several MetS indices. A clinical phase is proposed in this investigation to support and confirm the preclinical findings.