Hussin Muhammad

Background: Aflatoxin B1 (AFB1) is a potent hepatocarcinogen commonly found in staple foods from tropical regions. Aim: This scoping review collated existing evidence on AFB1 contamination in rice, maize, and peanut-based products across ASEAN countries to estimate chronic dietary exposure, Margin of Exposure (MOE), and the associated liver cancer risk. Methods: A systematic search was performed in five databases. Estimated Daily Intake (EDI) and risk metrics were calculated using sample-size weighted mean concentrations, along with regional consumption data. Risk characterisation used the benchmark dose lower confidence limit (BMDL₁₀) of 400 ng/kg BW/day, while liver cancer potency levels were adjusted according to Hepatitis B virus (HBV) prevalence for each population. Results: Twenty studies from Malaysia, Thailand, Vietnam, and the Philippines met the inclusion criteria. Peanuts and maize had the highest AFB1 concentrations among all food groups. Peanuts showed the highest contamination in the Philippines, followed by Malaysia, Vietnam, and Thailand. Maize exhibited a similar trend, with the highest levels observed in the Philippines. Most MOE values calculated were below 10,000, indicating a major public health concern. An exception was peanuts in Thailand, where MOE values exceeded 10,000, thus indicating a lower genotoxic carcinogenicity risk. The estimated liver cancer burden due to dietary AFB1 varied widely among countries and commodities. Conclusions: These findings show significant differences in AFB1 exposure in the ASEAN region. There is a need for improved surveillance, better post-harvest management, and harmonised regional risk management strategies.

The global increase in neurodegenerative disorders such as Alzheimer’s disease has prompted the search for effective non-pharmacological interventions. Chrono-exercise which is the physical training aligned with circadian rhythms has emerged as a novel strategy to strengthen cognitive resilience. This study explores the impact of chrono-exercises, incorporating aerobic, resistance, and combined modalities, performed at the early dark (ZT13) and early light (ZT1) phases in an aluminum chloride (AlCl ₃ )-induced rat model of neurodegeneration. One hundred male Wistar rats aged 2–3 months will undergo structured exercise interventions following AlCl ₃ exposure. Neurobehavioural assessments including novel object recognition and open-field tests along with grip strength analysis, biochemical profiling and histological evaluations of brain and muscle tissues will be conducted. We hypothesize that the timing of combined aerobic-resistance exercise critically influences neuroplasticity and cognitive performance. Findings are expected to guide circadian-based exercise prescriptions to counter cognitive decline and enhance brain health in aging populations.

Background/Objective: Current treatments for peripheral nerve injury (PNI) lack robust evidence to suggest complete recovery; hence, alternative therapeutics offer new opportunities to develop more effective protocols. Mushroom species and their related components are considered potential candidates for peripheral nerve repair, but their specific effects and underlying mechanisms are not fully understood. This systematic review presents the available evidence on the use of mushroom species for PNI therapy, including the bioactive components and mechanisms of action. Methodology: A comprehensive literature search in three databases (PubMed, Scopus, and Google Scholar) led to the synthesis of 11 records published between 2010 and 2024. Qualitative analysis revealed the neuroregenerative potential of four mushrooms: Amanita muscaria (n = 2), Hericium erinaceus (n = 5), Lignosus rhinocerotis (n = 3), and Flammulina velutipes (n = 1), with aqueous extracts as the most common type of ingredients used (n = 4) relative to specific components such as muscimol, polysaccharide, Erinacine S, and nerve-guided conduits (NGCs). Results: These mushroom-derived treatments enhanced the migration of Schwann cells mainly via the FGF-2 signalling and MAPK pathway. In vivo studies also revealed the ability of H. erinaceus, A. muscaria, and L. rhinocerotis to promote peripheral nerve repair and functional recovery, with evidence suggesting the role of neurotrophic factors, anti-apoptotic signalling, and pro-inflammatory substances. H. erinaceus was identified as the most promising for potential clinical applications, given the stronger evidence-based data and its relatively safer components compared to A. muscuria and other mushroom species. Conclusions: Despite presenting the potential use of mushrooms in managing PNIs, the existing approaches need to be subjected to clinical research to accelerate the development of future therapeutics and preventive measures for PNIs.

Sciatic nerve injury (SNI) is neurological condition that affecting the motor and sensory functions of muscles, characterized by the Wallerian degeneration and regeneration myelin axon. Motor neuron injuries result in muscle weakness and atrophy, sensory neuron damage impairs sensation, and autonomic injuries lead to organ dysfunction. This study investigates the potential effects of Clitoria ternatea nanoemulsion with different dosage (250 mg/kg, 500 mg/kg and 1,000 mg/kg) on Sprague Dawley (SD) rats that induced with sciatic nerve crush injury. Sciatic nerve crush injury was induced on SD rats using modified Watchmaker’s forceps for 15 seconds. On day 14 and 28, behaviour analysis of motor and sensory test was evaluated to assess the functional recovery. On day 28, the muscles were weight and stained with Haematoxylin & Eosin, while sciatic nerve were stained using Cresyl violet, Toluidine blue and TEM. The outcome of the treatment shown an improvement in functional recovery in the motor and sensory test. Additionally, the histomorphometry examination shows the same pattern as the behaviour analysis, increased in the degree maturity of the regenerated nerve fibres which resulting more axonal growth and thicker myelin. In conclusion, CT nanoemulsion treatment in high dose treatment shows promising potential treatment in treating sciatic nerve injury by improving functional recovery and myelin integrity.

The present study aimed to assess the potential maternal toxicity of Ficus deltoidea var. kunstleri aqueous extract in pregnant rats, along with its impact on maternal hepatic drug metabolism and foetal skeletal development. Pregnant rats were divided into five groups and orally administered varying doses of F. deltoidea aqueous extract (0, 250, 500, 1000, and 2000 mg/kg body weight) from gestation day 6 to 20. Throughout the administration period, clinical observations, body weight, and food and water intake were monitored. On gestation day 21, the pregnant rats were sacrificed, and their vital organs and foetuses were collected for analysis. Gene expression related to hepatic drug metabolism was evaluated using the RT2 Profiler™ PCR array. Foetal external morphology was examined for abnormalities, and skeletal structures were stained with Alizarin Red to assess the effects of F. deltoidea aqueous extract on bone ossification during organogenesis. No maternal toxicity was observed, except for a significant increase in liver weight in the treated groups (p < 0.05). Analysis of 84 genes revealed significant changes in 15, 4, and 11 genes in the 250, 500, and 2000 mg/kg body weight groups, respectively. Notably, Gpx5 and Pkm, both phase II metabolising enzyme genes were downregulated in a dose-dependent manner. Despite some skeletal variations, the extract did not induce foetal external malformations or skeletal abnormalities. The significant increase in maternal liver weight, together with the downregulation of Gpx5 and Pkm, suggests an adaptive hepatic response to the extract rather than an adverse effect. These findings also suggest that F. deltoidea var. kunstleri aqueous extract does not cause embryo toxicity, foetal growth retardation, or developmental malformations, particularly in skeletal formation. The developmental no-observed-adverse-effect level (NOAEL) was determined to be >2000 mg/kg/day via oral administration. Further research is warranted to explore the synergistic interactions of genes involved in hepatic drug metabolism in response to the extract.

Chronic stress is a key risk factor for depression and metabolic dysfunction, widely mediated through oxidative stress and inflammatory pathways. Natural products such as honey are increasingly investigated for their potential to attenuate stress-induced pathophysiological changes. This study evaluated the protective effects of Malaysian Acacia honey (AH) on glucose regulation, oxidative damage, histopathological alterations, and pro-inflammatory cytokine expression in stress-induced rats. Male Sprague–Dawley rats (n = 42) were subjected to chronic unpredictable mild stress and supplemented with AH, amitriptyline (AMT), or their combination for 28 days. Blood glucose levels, erythrocyte hemolysis, histological changes in liver and kidney, and expression of IL-1β and TGF-β1 in ileum, caecum, and hypothalamus were assessed. Data were reported as mean and standard error of mean (SEM) after three or more independent experiments had been conducted. The data were analyzed using a paired-t-test or a one-way or two-way analysis of variance (ANOVA) and considered significant if p < 0.05. Stress markedly elevated glucose levels (7.97 ± 0.20 mmol/L), increased hemolysis (14.30% ± 2.96), and induced hepatic (cytoplasmic vacuolation, 1.40 ± 0.25; cell lining absent, 1.20 ± 0.37) and renal lesions (dilated intertubular capillaries, 1.40 ± 0.51; inflammation, 2.20 ± 0.20), accompanied by upregulation of IL-1β (1.27-fold ± 0.20) and TGF-β1 (1.00-fold ± 0.08). Supplementation with AH significantly reduced hyperglycemia, inhibited hemolysis, ameliorated tissue damage, and downregulated pro-inflammatory cytokines. Combination therapy with AH and AMT produced the most significant improvements near to normal level, suggesting synergistic benefits. These findings highlight the therapeutic potential of AH as a natural adjunct in managing stress-related metabolic and inflammatory disturbances.

Introduction: Dioscorea hispida has been widely known for consumption as food due to its medicinal properties. The present study evaluated the safety of D. hispida tuber aqueous extract through single-dose toxicity and genotoxicity assessments. Methods: An acute oral toxicity study was conducted with single oral doses of 5, 50, 300, and 2000 mg/kg body weight D. hispida aqueous extract in respective groups. The bacterial reverse mutation test was performed on Salmonella typhimurium strains TA100, TA1535, TA98, TA1537, and Escherichia coli strain WP2uvrA using the pre-incubation method, both in the presence and absence of an exogenous metabolic activation system (S9). An in vitro micronucleus assay was carried out on V79B cells, a fibroblast-like cells. The cells were treated with D. hispida aqueous extract at concentrations of 1.25, 2.5, and 5 mg/ml, along with positive or negative controls (distilled water). The cells were stained with acridine orange, observed under a fluorescence microscope, and scored for micronuclei.Results: Our findings showed the administration of D. hispida aqueous extract did not cause any adverse effects up to 2000 mg/kg body weight. Additionally, D. hispida aqueous extract did not induce mutagenicity in tested Salmonella and E. coli tester strains and did not increase revertant colonies at concentrations up to 5000 μg/plate. No significant changes were observed in the number of micronucleated cells compared to the untreated group.Discussion: D. hispida aqueous extract is not toxic in both in vivo acute toxicity and in vitro genotoxicity studies. However, further investigations are needed for preclinical studies on repeated administration and in vivo genotoxicity assays.