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Garlic, an Allium vegetable, contains rich flavonoids organosulfur compounds (OSCs) that have potent anticancer properties. The aim of the review is to provide an overview of the different types of garlic, their active compounds, and the potential anticancer benefits with a focus on antioxidant activity. Animal and cell line studies have provided convincing evidence that garlic and its organosulfur compounds inhibit carcinogenesis through a number of events including induction of apoptosis, inhibiting cellular proliferation, scavenging radical oxygen species (ROS), increasing the activities of enzymes such as glutathione S -transferase, and reducing tumor size. Epidemiological studies showed compelling evidence that garlic consumption is associated with decreased risk of colorectal cancer, but inconsistent evidence for stomach, breast, and prostate cancers. Studies also suggest that the presence and potency of garlic OSCs varies with respect to the preparation and form of garlic. Further epidemiological studies with information on garlic form consumed or preparation methods and molecular studies regarding its antioxidant mechanisms, such as increasing enzymatic and nonenzymatic antioxidants levels, are warranted.

Atherosclerosis is a complex condition that involves the accumulation of lipids and subsequent plaque formation in the arterial intima. There are various stimuli, cellular receptors, and pathways involved in this process, but oxidative modifications of low-density lipoprotein (ox-LDL) are particularly important in the onset and progression of atherosclerosis. Ox-LDLs promote foam-cell formation, activate proinflammatory pathways, and induce smooth-muscle-cell migration, apoptosis, and cell death. One of the major receptors for ox-LDL is LOX-1, which is upregulated in several cardiovascular diseases, including atherosclerosis. LOX-1 activation in endothelial cells promotes endothelial dysfunction and induces pro-atherogenic signaling, leading to plaque formation. The binding of ox-LDLs to LOX-1 increases the generation of reactive oxygen species (ROS), which can induce LOX-1 expression and oxidize LDLs, contributing to ox-LDL generation and further upregulating LOX-1 expression. This creates a vicious circle that is amplified in pathological conditions characterized by high plasma levels of LDLs. Although LOX-1 has harmful effects, the clinical significance of inhibiting this protein remains unclear. Further studies both in vitro and in vivo are needed to determine whether LOX-1 inhibition could be a potential therapeutic target to counteract the atherosclerotic process.

Background: The incidence of glycolipid metabolic diseases is extremely high worldwide, which greatly hinders people’s life expectancy and patients’ quality of life. Oxidative stress (OS) aggravates the development of diseases in glycolipid metabolism. Radical oxygen species (ROS) is a key factor in the signal transduction of OS, which can regulate cell apoptosis and contribute to inflammation. Currently, chemotherapies are the main method to treat disorders of glycolipid metabolism, but this can lead to drug resistance and damage to normal organs. Botanical drugs are an important source of new drugs. They are widely found in nature with availability, high practicality, and low cost. There is increasing evidence that herbal medicine has definite therapeutic effects on glycolipid metabolic diseases. Objective: This study aims to provide a valuable method for the treatment of glycolipid metabolic diseases with botanical drugs from the perspective of ROS regulation by botanical drugs and to further promote the development of effective drugs for the clinical treatment of glycolipid metabolic diseases. Methods: Using herb*, plant medicine, Chinese herbal medicine, phytochemicals, natural medicine, phytomedicine, plant extract, botanical drug, ROS, oxygen free radicals, oxygen radical, oxidizing agent, glucose and lipid metabolism, saccharometabolism, glycometabolism, lipid metabolism, blood glucose, lipoprotein, triglyceride, fatty liver, atherosclerosis, obesity, diabetes, dysglycemia, NAFLD, and DM as keywords or subject terms, relevant literature was retrieved from Web of Science and PubMed databases from 2013 to 2022 and was summarized. Results: Botanical drugs can regulate ROS by regulating mitochondrial function, endoplasmic reticulum, phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT), erythroid 2-related factor 2 (Nrf-2), nuclear factor κB (NF-κB), and other signaling pathways to improve OS and treat glucolipid metabolic diseases. Conclusion: The regulation of ROS by botanical drugs is multi-mechanism and multifaceted. Both cell studies and animal experiments have demonstrated the effectiveness of botanical drugs in the treatment of glycolipid metabolic diseases by regulating ROS. However, studies on safety need to be further improved, and more studies are needed to support the clinical application of botanical drugs.

Salinity is a natural and anthropogenic process that plants overcome using various responses. Salinity imposes a two-phase effect, simplified into the initial osmotic challenges and subsequent salinity-specific ion toxicities from continual exposure to sodium and chloride ions. Plant responses to salinity encompass a complex gene network involving osmotic balance, ion transport, antioxidant response, and hormone signaling pathways typically mediated by transcription factors. One particular transcription factor mega family, WRKY, is a principal regulator of salinity responses. Here, we categorize a collection of known salinity-responding WRKYs and summarize their molecular pathways. WRKYs collectively play a part in regulating osmotic balance, ion transport response, antioxidant response, and hormone signaling pathways in plants. Particular attention is given to the hormone signaling pathway to illuminate the relationship between WRKYs and abscisic acid signaling. Observed trends among WRKYs are highlighted, including group II WRKYs as major regulators of the salinity response. We recommend renaming existing WRKYs and adopting a naming system to a standardized format based on protein structure.

This article focuses on the role that oxidative stress plays in chronic prostatitis, not only with respect to the known impact on symptoms and fertility but also especially in relation to possible prostate cancer development. Prostatitis is the most common urologic disease in adult males younger than 50 years and the third most common urologic diagnosis in males older than 50 years. If the germ-causing acute prostatitis is not eliminated, the inflammatory process becomes chronic. Persistent inflammation causes ongoing production of large quantities of pro-inflammatory cytokines and both oxygen and nitrogen reactive species, with consequent activation of transcription factor nuclear factor-kappa B (NF-κB) and genes encoding for further production of pro-inflammatory cytokines, chemotactic factors, and growth factors. Confirming the role of oxidative stress in chronic prostatitis, several studies have demonstrated the presence of oxidative stress markers in the genital secretions of patients suffering from the disease. Antioxidants can therefore play an essential role in the treatment of chronic bacterial and non-bacterial prostatitis; in the case of bacterial inflammation, they can be associated with antibiotic therapy. Moreover, due to their anti-inflammatory properties, antioxidants hinder the progression of inflammation and the possible development of prostate cancer.

The cultivation of rice is widespread worldwide, but its growth and productivity are hampered by heavy metals stress. However, sodium nitroprusside (SNP), a nitric oxide donor, has been found to be effective for imparting heavy metals stress tolerance to plants. Therefore, the current study evaluated the role of exogenously applied SNP in improving plant growth and development under Hg, Cr, Cu, and Zn stress. For this purpose, heavy metals stress was induced via the application of 1 mM mercury (Hg), chromium (Cr), copper (Cu), and zinc (Zn). To reverse the toxic effects of heavy metals stress, 0.1 mM SNP was administrated via the root zone. The results revealed that the said heavy metals significantly reduced the chlorophyll contents (SPAD), chlorophyll a and b, and protein contents. However, SNP treatment significantly reduced the toxic effects of the said heavy metals on chlorophyll (SPAD), chlorophyll a and b, and protein contents. In addition, the results also revealed that heavy metals significantly increased the production of superoxide anion (SOA), hydrogen peroxide (H2O2), malondialdehyde (MDA), and electrolyte leakage (EL). However, SNP administration significantly reduced the production of SOA, H2O2, MDA, and EL in response to the said heavy metals. Furthermore, to cope with the said heavy metals stress, SNP administration significantly enhanced the activities of superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and polyphenol peroxidase (PPO). Furthermore, in response to the said heavy metals, SNP application also upregulated the transcript accumulation of OsPCS1, OsPCS2, OsMTP1, OsMTP5, OsMT-I-1a, and OsMT-I-1b. Therefore, SNP can be used as a regulator to improve the heavy metals tolerance of rice in heavy-metals-affected areas.

Severe physical injuries and associated traumatic brain injury and/or hemorrhagic shock (HS) remain leading causes of death worldwide, aggravated by accompanying extensive inflammation. Retrospective clinical data indicated an association between mild hyperoxemia and improved survival and outcome. However, corresponding prospective clinical data, including long-term resuscutation, are scarce. Therefore, the present study explored the effect of mild hyperoxemia for 24 hours in a prospective randomized controlled trial in a long-term resuscitated model of combined acute subdural hematoma (ASDH) and HS. ASDH was induced by injecting 0.1 ml × kg −1 autologous blood into the subdural space and HS was triggered by passive removal of blood. After 2 hours, the animals received full resuscitation, including retransfusion of the shed blood and vasopressor support. During the first 24 hours, the animals underwent targeted hyperoxemia (P a O 2 = 200 – 250 mmHg) or normoxemia (P a O 2 = 80 – 120 mmHg) with a total observation period of 55 hours after the initiation of ASDH and HS. Survival, cardiocirculatory stability, and demand for vasopressor support were comparable between both groups. Likewise, humoral markers of brain injury and systemic inflammation were similar. Multimodal brain monitoring, including microdialysis and partial pressure of O 2 in brain tissue, did not show significant differences either, despite a significantly better outcome regarding the modified Glasgow Coma Scale 24 hours after shock that favors hyperoxemia. In summary, the present study reports no deleterious and few beneficial effects of mild targeted hyperoxemia in a clinically relevant model of ASDH and HS with long-term resuscitation in otherwise healthy pigs. Further beneficial effects on neurological function were probably missed due to the high mortality in both experimental groups. The present study remains exploratory due to the unavailability of an a priori power calculation resulting from the lack of necessary data.

Pharmaceutical residues are emerging contaminants of growing concern due to their persistence and poor removal efficiency in conventional wastewater treatment plants. This study evaluates UVC photolysis with type C ultraviolet radiation (UVC) and UVC/TiO2 photocatalysis of a mixture of four pharmaceuticals—atenolol (ATL), acetaminophen (ACM), clofibric acid (CLA), and antipyrine (ANT)—commonly found in treated urban wastewater. A comprehensive kinetic model was developed to describe their degradation, taking into account the generation of reactive oxygen species (ROS): hydroxyl (HO●), superoxide ion (O2●−) radicals, and singlet oxygen (1O2), along with their reactions with both the pharmaceuticals and dissolved organic matter. Direct quantum yields were determined as 8.05 × 10−3 mol·Einstein−1 for ATL, 1.93 × 10−3 for ACM, 3.12 × 10−1 for CLA, and 5.12 × 10−2 for ANT. In addition, rate constants of the reactions between singlet oxygen and pharmaceuticals were 9.93, 1.3 × 106, 1.18 × 102, and 1.14 × 104 M−1s−1 for ATL, ACM, CLA, and ANT, respectively. Scavenger experiments confirmed the key role of the ROS involved. The model reproduces the inhibitory effect of natural organic matter in secondary effluent and, in most cases, treated, accurately predicts the concentration profiles of the pharmaceuticals. Under photocatalytic conditions (0.10 g·L−1 TiO2), all compounds were completely degraded in less than 15 min. This validated model provides a useful tool for understanding the degradation mechanisms of pharmaceutical mixtures and for supporting the design of effective water strategies based on photochemical processes.

The public widely uses kersen ( Muntingia calabura L) fruit for consumption and treatment because Kersen fruit has various vitamins, minerals, and secondary metabolite compounds that reduce free radicals. The purpose of this study was to see the effectiveness of kersen fruit as an antioxidant agent. In this study, the samples used were ethanol extract (EE), Aqueous ethanol fraction (EF), ethyl acetate fraction (EAF), and n-hexane (HF) fraction from kersen fruit ( Muntingia calabura L). The samples were evaluated by observing the antioxidant activity profile using various methods, i.e., nitric oxide, β-carotene bleaching assay, hydroxyl radicals, and iron chelating. The results of this study showed that the IC 50 values of EE (31.05 μg/mL), AEF (33.86 μg/mL), FEA (40.48 μg/ml) gave powerful antioxidant activity while HF showed weak results (459 μg/ml). In the nitric oxide method. The hydroxyl radical method with IC 50 values of 32.06 μg/mL (EE), 38.73 μg/mL (EF), 22.18 μg/mL (EAF) gave very strong activity, and 53.37 μg/mL (HF) with strong activity. The β-carotene bleaching method gave powerful antioxidant activity results with IC 50 values <50 μg/mL in each sample. The Iron Chelation method showed weak antioxidant activity (IC 50 > 200 μg/mL) of each sample. Based on the results obtained, it can be concluded that the antioxidant activity of extracts and fractions in kersen fruit has a different activity profile according to the test method used.

Magnetic CuFe2O4 was prepared with the modified sol–gel method and used for enhanced peroxymonosulfate (PMS) activation and ofloxacin (OFL) degradation. The OFL could almost degrade within 30 min at a catalyst dosage of 0.66 g/L, PMS concentration of 0.38 mM, and initial pH of 6.53 without adjustment, using response surface methodology (RSM) with Box-Behnken design (BBD). In the CuFe2O4/PMS system, the coexisting substances, including CO32−, NO3−, SO42−, Cl− and humic acid, have little effect on the OFL degradation. The system also performs well in actual water, such as tap water and surface water (Mei Lake), indicating the excellent anti-interference ability of the system. The cyclic transformation between Cu(II)/Cu(I) and Fe(III)/Fe(II) triggers the generation of active radicals including SO4•−, •OH, •O2− and 1O2. The OFL degradation pathway, mainly involving the dehydrogenation, deamination, hydroxylation, decarboxylation and carboxylation processes, was proposed using mass spectroscopy. Moreover, the toxicity assessment indicated that the end intermediates are environmentally friendly. This study is about how the CuFe2O4/PMS system performs well in PMS activation for refractory organic matter removal in wastewater.