Sofian Abdul-Nasir

Alzheimer’s disease (AD) is a neurodegenerative condition in which amyloid-beta (Aβ) plaques trigger oxidative stress (OS) and neuroinflammation, causing memory loss. OS and neurodegeneration can also be caused by reactive astrocytes, thereby promoting AD via toxic metabolite accumulation in the astrocytic urea cycle. However, the effect of molecular hydrogen (H₂) on this cycle remains unknown. Therefore, we investigated whether H₂ treatment could reduce OS-induced neurodegeneration and memory loss. 5xFAD (n = 14) and wild-type (n = 15) mice were randomized into four groups and treated with either 3% hydrogen gas (H₂) or vehicle for 60 days. Cognitive behaviors were evaluated using the Morris water maze and Y-maze tests. In addition, we used biochemical assays to measure ammonia and hydrogen peroxide (H₂O₂) levels in the hippocampi of the mice and AβO-treated primary mouse astrocytes. Aβ, γ-aminobutyric acid (GABA), and the expression of inflammatory markers were evaluated using immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (qRT-PCR). We observed that H₂ treatment significantly prevented cognitive deficits, oxidative stress, the accumulation of toxic metabolites, and the increase in inflammatory markers in 5xFAD mice. These results suggest that H₂ therapy can mitigate toxic metabolites in the astrocytic urea cycle, thereby reducing neurodegeneration and memory loss in AD.

Background: Modulating ethanol metabolism and attenuating alcohol-induced oxidative stress are promising therapeutic strategies for reducing the severity of hangovers and alleviating their associated physiological burden. Methods: A randomized, double-blind, placebo-controlled, crossover study was conducted to evaluate the effects of the probiotic strain Leuconostoc mesenteroides VITA-PB2 on ethanol metabolism, oxidative stress, and hangover-related symptoms in 28 healthy adults. The participants consumed either VITA-PB2 or a placebo before standardized alcohol intake, with a 7-day washout period and subsequent crossover. Primary outcomes included blood ethanol, acetaldehyde levels, and aldehyde dehydrogenase (ALDH) activity. Secondary outcomes measured hangover severity assessed by the Acute Hangover Scale (AHS), liver enzymes including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT), oxidative stress indicators reactive oxygen species (ROS) and nitric oxide (NO), and antioxidant responses measured by glutathione peroxidase (GPx), catalase, and 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging capacity. Results: VITA-PB2 supplementation led to a sustained reduction in blood ethanol concentrations beginning at 0.5 h post-ingestion compared with the placebo group, indicating more efficient ethanol clearance. Additionally, VITA-PB2 significantly reduced acetaldehyde levels at 1 h post-ingestion (p < 0.05) and increased ALDH activity by 42.15% at 30 min (p < 0.05). It also markedly reduced ROS levels at 1 h (p < 0.05), enhanced glutathione peroxidase (GPx) activity at 2 h (p < 0.01), and significantly improved the subjective hangover symptoms, particularly thirst (p < 0.05). Conclusions: No adverse effects were reported during the trial, indicating that Leuconostoc mesenteroides VITA-PB2 is a safe probiotic. These findings suggest its efficacy in mitigating alcohol-induced oxidative stress and alleviating hangover-related symptoms.

Plywood and particle boards, commonly used in construction and interior environments, are sources of indoor chemical emissions from synthetic adhesives, resins, and surface treatments. Among these, formaldehyde, classified as a group 1 carcinogen by the International Agency for Research on Cancer, and other compounds are associated with oxidative stress, inflammation, and organ toxicity. This study aimed to evaluate the toxicological and physiological effects of plywood and particleboard emissions in female C57BL/6 mice. The mice were exposed to formaldehyde, phytoncides, and untreated wood samples under short- (30–60 days) and long-term (120–180 days) conditions. Biological effects were assessed through histopathology of major organs, differential white blood cell counts, oxidative stress markers, antioxidant enzyme activities (catalase and glutathione peroxidase), liver and kidney function tests (alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, and creatinine), and inflammatory cytokine profiling (interferon-gamma, tumor necrosis factor-α, interleukin (IL)-10, and IL-12p70). These findings revealed no significant pathological changes or systemic toxicity following long-term exposure. Minor elevations in hepatic and renal biomarkers were observed but remained within physiological limits. Antioxidant responses and cytokine fluctuations suggested mild adaptive and immunomodulatory effects. These results highlight the importance of reducing emissions from engineered wood products to improve indoor air quality and minimize potential health risks.

Airway inflammatory diseases, such as asthma, are a global public health concern owing to their chronic inflammatory effects on the respiratory mucosa. Molecular hydrogen (H₂) has recently been recognized for its antioxidant and anti-inflammatory properties. In this study, we examined the therapeutic potential of H₂ in airway inflammation using an ovalbumin (OVA)-induced BALB/c mouse model of allergic asthma. Female BALB/c mice were sensitized and challenged with OVA to induce airway inflammation, and 30 mice were randomly divided into five groups: NT (non-treatment), HTC (3% H₂ treatment only), NC (negative control, OVA only), PC (positive control, OVA + intranasal 1 mg/mL salbutamol 50 μL), and HT (H₂ treatment, OVA + inhaled 3% H₂). Various inflammatory and oxidative stress (OS)-induced markers such as white blood cells (WBCs) and their differential counts, lung histology, cytokine levels such as interleukin (IL)-4, (IL)-5, (IL)-13, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), (IL)-10, reactive oxygen species (ROS), nitric oxide (NO), glutathione peroxidase (GPx), and catalase (CAT), and total immunoglobulin E (IgE) levels were investigated. Our results showed that inhaled H₂ significantly reduced inflammatory cell infiltration, OS markers, and pro-inflammatory cytokine expression while upregulating antioxidant enzyme activity. Furthermore, H₂ also significantly decreased serum IgE levels, a marker of allergic inflammation. Collectively, our findings suggest that H₂ inhalation is a promising treatment option for airway inflammation, offering a novel approach with potential clinical applications.

Cervical and prostate cancer account for 7.1 and 7.3 deaths per 100,000 people globally in 2022. These rates increased significantly to 17.6 and 17.3 in Africa, respectively, making them the second and third leading cause of cancer deaths in Africa, only surpassed by breast cancer. The human papillomavirus is the prime risk factor for cervical cancer infection. On the other hand, prostate cancer risks include ageing, genetics, race, geography, and family history. However, these factors alone cannot account for the high mortality rate in Africa, which is more than twice the global mortality rate for the two cancers. We searched PubMed, Embase, Scopus, and Web of Science to select relevant articles using keywords related to microorganisms involved in cervical and prostate cancer and the impact of poor healthcare systems on the mortality rates of these two cancers in Africa by carrying out a detailed synopsis of the studies on microbial agents involved and the contributory factors to the deteriorating healthcare system in Africa. It became apparent that the developed countries come first in terms of the prevalence of cervical and prostate cancer. However, more people per capita in Africa die from these cancers as compared to other continents. Also, microbial infections (bacterial or viral), especially sexually transmitted infections, cause inflammation, which triggers the pathogenesis and progression of these cancers among the African population; this has been linked to the region’s deficient health infrastructure, making it difficult for people with microbial infections to access healthcare and hence making infection control and prevention challenging. Taken together, untreated microbial infections, primarily sexually transmitted infections due to the deficient healthcare systems in Africa, are responsible for the high mortality rate of cervical and prostate cancer.

CfDNA is known to be a beneficial biomarker for the diagnosis, treatment response, and prognosis of sepsis. Previous cell line studies have shown that cfDNA in septic mice triggers inflammatory responses and tissue damage, and the mechanism occurs by binding to toll-like receptors (TLRs). Meanwhile, reactive oxidative species (ROS) and nitric oxide (NO) are increased in sepsis, which is known to be associated with organ failure and poor prognosis of sepsis through immunoredox imbalance. This study investigates the occurrence and mechanisms of inflammatory responses when cfDNA from septic mice is administered to macrophages (RAW 264.7 cells) and normal ICR mice aged 7-9 weeks. In addition, cfDNA-activated genes and their pathways are investigated and studied. Tumor necrosis factor-alpha (TNF-α) measured 24 hours after administration of 100, 200, and 400 ng/mL of sepsis-derived cfDNA to healthy mice was significantly higher in the 400 ng/mL group than in the control group. Furthermore, in macrophage cell line experiments, total ROS, NO, and catalase concentrations measured at 24 hours after cfDNA administration were significantly increased compared to the control group. In the meantime, cell viability studies revealed that the viability of the group treated with cfDNA from septic mice was much lower than that of the control group treated with normal human cfDNA. Cytokine levels such as granulocyte colony-stimulating factor (G-CSF), tumor necrosis factor-alpha (TNF-σ), interleukin-10 (IL-10), and vascular endothelial growth factor (VEGF) were significantly higher in the 5 ng/mL group when compared to the 1 ng/mL group, but levels of IL-1β and IL-6 were not significantly higher. Finally, we measured the expression levels of several oxidative stress genes and receptor (TLR) genes and found that 46 cytokines & chemokines genes, namely II23a, Cxc10, XcI1, Csf1, Tnfsf10, Tnf, II10, Tgfb2, Ltb, II15, CcI22, Cd70, Cc15, Lta, CxcI11, Cntf, Ctf1, Bmp6, II11, II22, II24, II27, CxcI12, Ccl7, Tnfsf11, Gapdh, Hprt, Ppia, RpI13a, Tbp, Spp1, Cd40lg, Cxcl3, Cxcl1, lfng, Thpo, Ppbp, II5, II13, Fasl, Ccl11, Bmp4, Ccl4, Cxc19, Adipoq and Tnfrs11b and 18 oxidative stress genes, namely Sod3, Gpx1, Ucp2, Krt1, Cygp, II19, Rag2, Epx, Hspa1a, Psmb5, Prdx2, Txn1, Ngb, Nox4, Ercc2, Ncf2, Noxo1, and Ptgs1 were expressed at various levels, and 13 receptor genes, namely Sod3, Gpx1, Cd80, NfkbiL1, Tlr3, II2, Eif2ak2, II6ra, Hmgb1, Chuk, Tirap, Tradd, and Mapk8ip3, were also expressed at various levels. cfDNA from septic mice and healthy humans exhibit different immunoredox responses through immunoredox-related gene pathways.

Diabetes, a chronic metabolic disorder, affects glucose consumption in the body and leads to severe kidney damage, known as diabetic nephropathy, where oxidative stress (OS) plays a vital role in disease pathogenesis. Electrolyzed weakly alkaline reduced water (EWARW) is known to have anti-oxidative functions in vitro due to its bioactive properties. However, there is an increasing need for adequate research on EWARW-specific therapies to minimize the negative consequences of hyperglycemia-induced OS in the kidney. This study aimed to determine the anti-oxidative and anti-diabetic effects of EWARW at pH 8.5 on human kidney-2 (HK-2) cells. Here, HK-2 cells were treated with 71.68 mM glucose to induce OS and then treated with 10% tap water (TW)_7.7, electrolyzed alkaline reduced water (EARW)_9.5, or EARW_8.5 for 24 h. After treatment, cell viability, OS and apoptotic markers, glucose uptake, adenosine triphosphate (ATP) content, and inflammatory markers were assessed to determine the effect of EARW_8.5. Our results revealed that EARW_8.5 rescued cell viability in comparison to the high glucose (HG) only and TW_7.7 groups. In addition, EARW_8.5 was effective in reducing OS markers (ROS, NO, and CAT), apoptotic markers (cleaved caspase-3), mitogen-activated protein kinase (MAPK) markers (p-JNK and p-p38), diabetic markers (glucose uptake), and inflammatory markers (p-STAT1, p-STAT3, IL-1β, and IL-6). Furthermore, we found EARW_8.5 treatment enhanced GPx and ATP content in HG-induced HK-2 cells compared to the HG-only and TW_7.7 groups. Collectively, EARW_8.5 stabilized antioxidant defenses and modulated inflammation, improving cellular metabolism and rescuing HG-induced harmful effects in HK-2 cells.

Diabetes is coupled with hyperglycemia, a state in which elevated glucose levels trigger oxidative stress (OS) in various body functions. One of the organs most afflicted by diabetes is the kidney. Despite this, specific treatments to mitigate the harmful effects of hyperglycemia-induced OS in the kidney have not been extensively explored. This study evaluates the anti-hyperglycemic efficacy of magnesium-enhanced alkaline-reduced water (MARW) in human kidney-2 (HK-2) cells. OS, mitogen-activated protein kinase (MAPK) signaling and fibrosis markers were assessed in high glucose (HG)-induced HK-2 cells, followed by treatment with experimental water for 24 h. Surprisingly, MARW rescued the vitality of HG-induced HK-2 cells, in contrast to that seen with other experimental waters. Additionally, MARW maintained reactive oxygen species, nitric oxide, catalase, glutathione peroxidase, hepatocyte growth factor and glucose uptake in HG-induced HK-2 cells but not in tap water and mineral water. Similarly, MARW downregulated the expression of MAPK and fibrosis-linked signaling proteins such as p-p38, phospho-c-Jun N-terminal kinase, α-smooth muscle actin, matrix metalloproteinase-3 and cleaved caspase 3 in HG-induced HK-2 cells. In conclusion, MARW protects HK-2 cells from the deleterious effects of HG by stabilizing antioxidant defenses and by signaling cascades related to metabolism, apoptosis and fibrosis.