Temidayo Daniel Adeniyi

Background: The rising consumption of herbal alcoholic beverages in Nigeria, driven by unverified health claims, poses growing public health risks and adds to the global disease burden. Aim: To evaluate the effects of ascorbate and alpha-tocopherol supplementation on hepatorenal biochemical parameters, histopathology, and expression of oxidative stress-related genes (Nrf2 and CYP2E1) in rats exposed to a herbal-based alcoholic beverage. Methods: Twenty-eight adult male Wistar rats were randomly assigned into four groups (n=7 per group) using a computer-generated randomisation, with all outcome assessments performed under blinded conditions. Group I consisted of the unexposed control rats. Group II rats received a daily oral dose of alcohol at 0.2 mL/kg/bw. Groups III and IV were also administered alcohol daily at 0.2 mL/kg/bw but were additionally treated with ascorbate (500 mg/kg) and alpha-tocopherol (300 mg/kg), respectively, for 28 days. Hepatorenal biochemical parameters, hepatic and renal Nrf2 and CYP2E1 expression, and histopathological changes were subsequently evaluated. Results: Supplementation with ascorbate (500 mg/kg) or α-tocopherol (300 mg/kg) was associated with significantly lower (p < 0.05) ALP, ALT, AST, creatinine, and urea levels compared with alcohol-exposed untreated rats. Vitamin supplementation was associated with the modulation of alcohol-induced overexpression of CYP2E1 and Nrf2, and partially restored the altered biochemical parameters. Histopathological examination further revealed mitigated alcohol-induced architectural disruptions in the liver and kidney, suggestive of the protective effects of antioxidant supplementation. Conclusion: Ascorbate and alpha-tocopherol supplementation were associated with attenuation of alcohol-induced hepatorenal biochemical alterations, partial normalisation of liver and kidney function parameters, and modulation of oxidative stress-related gene expression (CYP2E1, Nrf2), findings consistent with a potential adjunctive role of these vitamins in mitigating alcohol-related organ toxicity rather than indicating definitive therapeutic effects. Mechanistic conclusions are limited by the absence of direct oxidative stress marker measurements (lipid peroxidation, glutathione status, antioxidant enzyme activities), and interpretation is limited by the absence of pure ethanol and vitamin-only control groups and the lack of independent chemical verification of the test beverage.

Environmental pollution remains a global health issue linked to numerous diseases, primarily through the generation of reactive oxygen species (ROS) that induce lipid peroxidation, protein and DNA damage, and cellular dysfunction. This review examines the therapeutic potential of medicinal ethnobotanicals in mitigating pollution-induced oxidative stress, with a focus on their molecular mechanisms and therapeutic potentials. Ethnobotanicals, rich in bioactive phytochemicals such as flavonoids, phenolic acids, alkaloids, and terpenoids, exhibit potent antioxidant and cytoprotective properties. Their protective effects are largely mediated through the enhancement of endogenous antioxidant systems and modulation of redox-sensitive signalling pathways. Evidence from both in vivo and in vitro studies highlights the efficacy of selected ethnobotanicals in reducing oxidative biomarkers and restoring tissue homeostasis, particularly in mammalian systems. This review highlights the potential of ethnobotanicals as promising agents in mitigating the health effects of environmental pollutants.

Pentazocine is an opioid used as an analgesic for treating moderate or severe pain. Its abusive use can trigger numerous deleterious effects. We examined the impact of pentazocine administration on the cerebellum of juvenile male mice, focusing on motor-social behaviours, lipid peroxidation, reduced glutathione, superoxide dismutase, catalase, myeloperoxidase, nitric oxide, cyclooxygenase-2, tumour necrosis factor alpha, and sodium-potassium pump (Na+/K+-ATPase), serotonin, dopamine, acetylcholinesterase, and butyrylcholinesterase, as well as mitochondrial functions in the cerebellum of juvenile male mice. The mice were administered 0.25 mL/kg, 0.5 mL/kg, and 0.75 mL/kg of pentazocine dissolved in sterile water for injection s.c. twice daily for 14 days. The results of this study revealed that exposure to pentazocine triggers upregulated activities of increased respective levels of lipid peroxidation, reduced glutathione, superoxide dismutase, catalase, myeloperoxidase, nitric oxide, cyclooxygenase-2, and tumour necrosis factor-alpha, respectively. Our data also showed that exposure to graded doses of pentazocine altered the respective levels of serotonin, dopamine, acetylcholinesterase, and butyrylcholinesterase, with a reduction in the activity of Na+/K+-ATPase. Our experiment further showed that exposure to pentazocine is linked to mitochondrial dysfunctions as well as neuronal degeneration in the cerebellum. Conclusively, our study reveals the significant neurotoxic effects of pentazocine, particularly on motor and social behaviour, along with notable biochemical and neuropathological changes in the cerebellar cortex. These findings suggest that the abusive use of pentazocine causes critical cellular and molecular alterations that contribute to neurotoxicity.

Access to clean water is necessary for human, animal, and environmental health. Anthropogenic human activities such as mining, agriculture, and continuous pollution from industrial waste, as well as population growth, continue to compromise the quality of water. The neurodegenerative impact of mercury with a similar concentration as obtained from waterways on the prefrontal cortex of Wistar rats was studied. Twenty adult rats were randomised into two groups: a control group and a 0.001 mg/L mercury (II) thiocyanate (Hg(SCN)2) group, ad libitum for 65 days, after which the animals were euthanised via cervical dislocation. Blood and tissue samples were obtained for analyses of oxidative stress biomarkers: superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA), hydrogen peroxide (H2O2), histological, and glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS) immunohistochemical evaluation. Statistical data were analysed using a t-test, set at p < 0.05. When comparing the mercury-treated groups to the control, a significant difference was observed in the SOD, GPx, MDA, and H2O2 values, with cellular alterations evident in the mercury-treated rats. Additionally, mercury treatment resulted in the distortion of the cortical histoarchitecture with intense immunoreactivity of GFAP and iNOS suggesting neuroinflammation. This study highlighted that mercury exposure induced oxidative stress and led to distortion in the histoarchitecture of the prefrontal cortex of adult Wistar rats.

Damilare Adedayo Adekomi, John Olabode Fatoki, Titilayo Deborah Adesipe, Omowumi Oyeronke Adewale, Adesina Oloruntoba Adekeye, Temidayo Daniel Adeniyi, Opeyemi Samson Osuntokun, Babatunde Joseph Dare, Lukman Adeayo Yunus, Olumayowa Kolawole Idowu, Ismail Adetayo Lawal, Fatima Omowumi Hamzat. Anat Cell Biol -0001;0:. https://doi.org/10.5115/acb.24.116

Petroleum-powered generators are commonly used in many developing countries as an alternative to meet utility demands. Generator exhaust emission significantly contributes to air pollution, which remains a constant threat to human health due to the presence of aromatic hydrocarbons and other harmful gases. This study assessed oxidative stress parameters in response to exhaust emission from gasoline generator engine in adult male wistar rats. Forty-eight (48) adult wistar rats weighing between 180-200g were randomly allocated to four (4) groups (A-D) of twelve (12) rats each. After the acclimatization period, the control group (A) were kept unexposed, whereas rats in groups (C-D) were exposed daily at 2, 4, and 8-hour intervals for 4, 8, and 12 weeks, respectively. Tissue samples were obtained at four weeks intervals. Fresh lung tissues weighing 1g were rinsed twice in phosphate-buffered saline (PBS, pH 8.0), homogenized and centrifuged at 3000 revolutions per minute for 20 min at 4°C. Supernatant levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), reduced glutathione (GSH), nitric oxide (NO), hydrogen peroxide (H2O2), catalase (CAT), and total antioxidant status (TAS) were determined using standard protocols. The findings revealed elevated oxidant levels of MDA, NO, and H2O2, whereas SOD, GPX, GST, GSH, CAT, and TAS were significantly reduced across the exposure time points compared to the unexposed control rats (p < 0.05). The research findings revealed that exposure to emissions from gasoline generators induced oxidative stress in the exposed rats, with the extent of disruption to their oxidative balance dependent on the duration and length of exposure time.

Highlights:1. This study provides insight into the detrimental effect of cadmium exposure on mammalian cells using a murine model.2. The co-administration of Rauvolfia vomitoria and Aframomum melegueta leaf extracts is more effective in ameliorating cadmium-induced toxicity than a single administration of each plant extract.3. The co-administration of Rauvolfia vomitoria and Aframomum melegueta plant extracts can upregulate the expression of IL-10 and reverse the derangements in the TNF-α, IL-6, SOD, and GPX levels. Abstract Cadmium has long been known to be an environmental pollutant that can harm human health, with toxicity majorly affecting the kidneys and liver. This study aimed to investigate the mitigating potential of methanol extracts of Rauvolfia vomitoria and Aframomum melegueta leaves in cadmium-induced liver toxicity. Twenty-five male adult Wistar rats, averagely weighing 200 g, were randomly allocated into five groups, each comprising five rats. Group 1 was unexposed to any substances and only received distilled water. Group 2 was given cadmium at a standard dose of 12 mg/kg bw. Groups 3, 4, and 5 received 12 mg/kg bw of cadmium, and each group was treated with 200 mg/kg bw of Rauvolfia vomitoria leaf extract, Aframomum melegueta leaf extract, and a combination of both extracts, respectively. After 28 days, the animals were euthanized to obtain their livers, which were then excised and processed for histopathological, mRNA expression, and biochemical analyses. A one-way analysis of variance (ANOVA) was used to analyze the data, and Duncan multiple tests were employed to compare the categorical variables (p<0.05). The results revealed elevated levels of interleukin 10 (IL-10) in the rats treated with Rauvolfia vomitoria and Aframomum melegueta extracts when compared to Group 2. On the other hand, the treatment groups exhibited a significant decrease in tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) levels, along with significantly elevated levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Group 5 showed a normal liver histoarchitecture similar to Group 1, reversing the histopathological abnormalities shown in Group 2. In conclusion, the co-administrative treatment using Rauvolfia vomitoria and Aframomum melegueta extracts reversed the cadmium-induced toxicity better than using each plant extract individually. This further suggests that Rauvolfia vomitoria and Aframomum melegueta leaf methanol extracts may ameliorate the effects of cadmium-induced toxicity, including reducing oxidative stress and fortifying the anti-oxidant system.

The unrestricted and unsystematic use of cypermethrin pesticides has detrimental effects on the organs, ranging from short-term sickness to long-term effects. The ameliorating effect of alpha-tocopherol and ascorbate was investigated singly and in combination with cypermethrin-induced oxidative stress using murine models. Additionally, the livers and kidneys of rats were histologically evaluated. Twenty-five (25) adult male Wistar rats with an average weight of 190 g were allocated randomly into five groups consisting of five rats each. Group I consists of the unexposed control rats, while rats in groups II-V were the test group exposed to cypermethrin at standard doses of 10 mg.kg-1 bw. While rats in group II were exposed and untreated, group III-V was administered with ascorbate (5000 mg.kg-1 bw), alpha-tocopherol (3000 mg.kg-1 bw), and co-administered with both vitamins at their standard doses, respectively. Regimen administration was by gavage for 28 days, and while the vitamins were administered daily, cypermethrin exposure was done twice a week. At the end of the experiment, rats were euthanized, and blood obtained via cardiac puncture was used for biochemical analysis, while the liver and kidneys excised were processed for histopathological evaluation. Results revealed elevated aspartate transferase (AST), alanine transferase (ALT), malondialdehyde (MDA), and creatinine levels. At the same time, a decrease in superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities was observed in the test group (p<0.05). Additionally, treatment with ascorbate and alpha-tocopherol co-administration reversed the biochemical parameters in the exposed rats. Conclusively, ascorbate and alpha-tocopherol ameliorate oxidative damage associated with cypermethrin exposure. Keywords: Cypermethrin, Histopathology, Pesticides, Toxicity, Vitamins.

Background: The application of pyrethroid pesticides to control pests has been widely implemented both domestically and industrially in Nigeria. Excessive and unregulated usage of pesticides can have toxic effects on the male reproductive system. Objectives: This study investigated the toxicological impact of Cypermethrin on the testes, as well as the potential mitigating effects of single and combinatorial administration of ascorbic acid and alpha-tocopherol in adult male Wistar rats. Methods: Twenty-five adult male Wistar rats weighing between 180 and 200g were randomly assigned to five groups of five rats each. Group I was the unexposed control group, while Group II was the Cypermethrin (10mg/kg/bw) exposed group. Groups III-V were exposed to Cypermethrin at standard doses of 10 mg/kg/bw and orally administered with ascorbic acid (5000mg/kg/bw), Alpha-tocopherol (3000mg/kg/bw), and coadministration of Ascorbic acid and Alpha-tocopherol respectively for 28 days. At the end of the experiment, the rats were euthanized, and their testes were harvested and processed for biochemical and histopathological analysis. Results: The findings revealed elevated malondialdehyde (MDA) levels, as well as a significant decrease in superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities (p < 0.05). There were no visible histological changes in the testes, and co-administration of ascorbic acid and alpha-tocopherol restored biochemical parameters better than single administration. Conclusion: Coadministration of ascorbic acid and alpha-tocopherol reduces cypermethrin-induced oxidative stress better than single administration, possibly due to their complementary antioxidant properties.