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Dietary exposures implicated as reducing or causing risk for colorectal cancer may reduce or cause DNA damage in colon tissue; however, no one has assessed this hypothesis directly in humans. Thus, we enrolled 16 healthy volunteers in a 4-week controlled feeding study where 8 subjects were randomly assigned to dietary regimens containing meat cooked at either low (100°C) or high temperature (250°C), each for 2 weeks in a crossover design. The other 8 subjects were randomly assigned to dietary regimens containing the high-temperature meat diet alone or in combination with 3 putative mutagen inhibitors: cruciferous vegetables, yogurt, and chlorophyllin tablets, also in a crossover design. Subjects were nonsmokers, at least 18 years old, and not currently taking prescription drugs or antibiotics. We used the Salmonella assay to analyze the meat, urine, and feces for mutagenicity, and the comet assay to analyze rectal biopsies and peripheral blood lymphocytes for DNA damage. Low-temperature meat had undetectable levels of heterocyclic amines (HCAs) and was not mutagenic, whereas high-temperature meat had high HCA levels and was highly mutagenic. The high-temperature meat diet increased the mutagenicity of hydrolyzed urine and feces compared to the low-temperature meat diet. The mutagenicity of hydrolyzed urine was increased nearly twofold by the inhibitor diet, indicating that the inhibitors enhanced conjugation. Inhibitors decreased significantly the mutagenicity of un-hydrolyzed and hydrolyzed feces. The diets did not alter the levels of DNA damage in non-target white blood cells, but the inhibitor diet decreased nearly twofold the DNA damage in target colorectal cells. To our knowledge, this is the first demonstration that dietary factors can reduce DNA damage in the target tissue of fried-meat associated carcinogenesis. ClinicalTrials.gov NCT00340743.

Residents of Qidong, People's Republic of China, are at high risk for development of hepatocellular carcinoma, in part from consumption of foods contaminated with aflatoxins. Chlorophyllin, a mixture of semisynthetic, water-soluble derivatives of chlorophyll that is used as a food colorant and over-the-counter medicine, has been shown to be an effective inhibitor of aflatoxin hepatocarcinogenesis in animal models by blocking carcinogen bioavailability. In a randomized, double-blind, placebo-controlled chemoprevention trial, we tested whether chlorophyllin could alter the disposition of aflatoxin. One hundred and eighty healthy adults from Qidong were randomly assigned to ingest 100 mg of chlorophyllin or a placebo three times a day for 4 months. The primary endpoint was modulation of levels of aflatoxin-N7-guanine adducts in urine samples collected 3 months into the intervention measured by using sequential immunoaffinity chromatography and liquid chromatography-electrospray mass spectrometry. This aflatoxin-DNA adduct excretion product serves as a biomarker of the biologically effective dose of aflatoxin, and elevated levels are associated with increased risk of liver cancer. Adherence to the study protocol was outstanding, and no adverse events were reported. Aflatoxin-N7-guanine could be detected in 105 of 169 available samples. Chlorophyllin consumption at each meal led to an overall 55% reduction (P = 0.036) in median urinary levels of this aflatoxin biomarker compared with those taking placebo. Thus, prophylactic interventions with chlorophyllin or supplementation of diets with foods rich in chlorophylls may represent practical means to prevent the development of hepatocellular carcinoma or other environmentally induced cancers.

To improve the tumor-targeting efficacy of photodynamic therapy, biotin was conjugated with chlorin e6 to develop a new tumor-targeting photosensitizer, Ce6-biotin. The Ce6-biotin had good water solubility and low aggregation. The singlet-oxygen generation rate of Ce6-biotin was slightly increased compared to Ce6. Flow cytometry and confocal laser scanning microscopy results confirmed Ce6-biotin had higher binding affinity toward biotin-receptor-positive HeLa human cervical carcinoma cells than its precursor, Ce6. Due to the BR-targeting ability of Ce6-biotin, it exhibited stronger cytotoxicity to HeLa cells upon laser irradiation. The IC50 against HeLa cells of Ce6-biotin and Ce6 were 1.28 µM and 2.31 µM, respectively. Furthermore, both Ce6-biotin and Ce6 showed minimal dark toxicity. The selectively enhanced therapeutic efficacy and low dark toxicity suggest that Ce6-biotin is a promising PS for BR-positive-tumor-targeting photodynamic therapy.

Chemical pesticides have been used as a reliable method of controlling pests on crops. However, their applications have led to the development of resistance, environmental problems, and risks to human health. Therefore, new chemicals in nanoform such as chlorophyll derivatives could be a good choice for pest control through the induction of reactive oxygen species, liberating singlet oxygen when they are excited by photo exposure. The present work evaluated the toxicity of magnesium chlorophyllin (Mg-Chl) and magnesium chlorophyllin zinc oxide (Mg-Chl–ZnO NC) nanocomposite on Spodoptera frugiperda (J.E. Smith) (Lepidoptera: Noctuidae) . Additionally, the biochemical changes of detoxifying enzymes, such as carboxylesterases (CXEs) and glutathione- S -transferases (GSTs), were investigated. In silico, molecular docking analysis was also performed to assess the binding affinities of the tested compounds to CXE22 and SfGSTe9 . Thus, the evaluation of potential photosensitizers against the second instar larvae of Chrysoperla carnea Stephens, as non-target insect and active predator of aphids, was conducted. The results showed that both Mg-Chl and Mg-Chl–ZnO NC have a high potency against S. frugiperda with LC 50  = 0.59 and 0.49 mg L −1 , respectively, after 12-h dark incubation and 5-h light exposure, while after 24 h, LC 50 values after dark incubation were 0.51 and 0.31 mg L −1 , respectively. Both tested compounds exhibited a strong binding affinity to CXE22 and SfGSTe9 , leading to significant alterations in CXEs activity and GSTs activity in correspondence with the oxidative stress and contributing to larval mortality. In parallel, both compounds exhibited very low toxicity on C. carnea . Overall, these findings support that Mg-Chl and Mg-Chl–ZnO NC could be used as alternative approaches to synthetic pesticides for the management of S. frugiperda .

Pancreatic cancer (PC) has high lethality due to multiple reasons, and its limited response to conventional chemotherapy like gemcitabine (GEM) is a non-negligible one. Therefore, our study introduces Chlorophyllin (CHL) as an effective therapeutic candidate to enhance the therapeutic efficacy of GEM. Our results demonstrate that the combination of CHL and GEM exhibits a significant synergistic anti-tumor effect by targeting multiple oncogenic processes in PC, including inhibiting cell proliferation, invasion, and migration, as well as inducing cell apoptosis. Further investigations of mechanism have revealed that CHL induces cuproptosis in PC cells through a multifaceted process, involving depleting cellular intracellular glutathione (GSH), increasing reactive oxygen species (ROS) levels, and subsequently upregulating the HSP70 protein in response to heightened oxidative stress. Additionally, CHL releases free Cu 2+ , binds to the Ferredoxin 1 (FDX1) protein, and ultimately leads to the oligomerization of Dihydrolipoamide S-Acetyltransferase (DLAT) proteins to amplify the copper toxicity within PC cells. Moreover, in vivo experiments have demonstrated that the combination of CHL and GEM effectively inhibits the growth of subcutaneously transplanted tumors while maintaining a favorable biosafety profile. In conclusion, our study identifies CHL as a potent enhancer of GEM’s anti-tumor effects in PC through the induction of cuproptosis, thus providing a novel therapeutic avenue for patients with PC.

Antimicrobial resistance in Cutibacterium acnes is a growing concern, limiting treatment options for acne vulgaris (AV) and increasing the risk of opportunistic infections. Photodynamic therapy (PDT), using an effective photosensitizer (PS) and optimized light parameters, is a potent broad-spectrum antimicrobial strategy with minimal risk of resistance development. This study aimed to assess the efficacy of PDT using sodium iron chlorophyllin (CHL-Fe) as an in-house photosensitizer (CH-PDT) against 10 clinically isolated, drug-resistant C. acnes strains. The isolates, obtained from patients with mild to severe AV in a dermatology referral center, were resistant to one or more commonly prescribed antibiotics. CH-PDT was conducted using varying concentrations of CHL-Fe and red light (RL) fluences in laboratory conditions. A consistent bactericidal activity (> 3 log 10 CFU/mL reduction) was achieved across all resistance profiles with a fixed dose of CHL-Fe at 7.5 mg/dL combined with RL at 3.5 J/cm². Neither CHL-Fe nor RL alone, even at higher doses, produced similar results. The study included pan-, extensively, multi-, and single-drug-resistant strains, making the findings broadly applicable to clinical practice. These findings underscore CH-PDT as a promising nonantibiotic therapy for drug-resistant AV, with potential implications for eradicating C. acnes colonization and preventing infections in surgical and implant-related settings.

Barium chloride (BaCl2), a known environmental pollutant, induces organ-specific oxidative stress through disruption of redox homeostasis. This study evaluated the protective effects and safety profile of sodium copper chlorophyllin (SCC) and ascorbic acid (ASC) against BaCl2-induced oxidative damage in the liver and brain of mice using a two-phase experimental protocol. Animals received either SCC (40 mg/kg), ASC (160 mg/kg), or their combination for 14 days prior to BaCl2 exposure (150 mg/L in drinking water for 7 days), allowing evaluation of both preventive and therapeutic effects. Toxicological and behavioral assessments confirmed the absence of systemic toxicity or neurobehavioral alterations following supplementation. Body weight, liver and kidney indices, and biochemical markers (Aspartate Aminotransferase (ASAT), Alanine Aminotransferase (ALAT), creatinine) remained within physiological ranges, and no anxiogenic or locomotor effects were observed. In the brain, BaCl2 exposure significantly increased SOD (+49%), CAT (+66%), GPx (+24%), and GSH (+26%) compared to controls, reflecting a robust compensatory antioxidant response. Although lipid peroxidation (MDA) showed a non-significant increase, SCC, ASC, and their combination reduced MDA levels by 42%, 37%, and 55%, respectively. These treatments normalized antioxidant enzyme activities and GSH, indicating an effective neuroprotective effect. In contrast, the liver exhibited a different oxidative profile. BaCl2 exposure increased MDA levels by 80% and GSH by 34%, with no activation of SOD, CAT, or GPx. Histological analysis revealed extensive hepatocellular necrosis, vacuolization, and inflammatory infiltration. SCC significantly reduced hepatic MDA by 39% and preserved tissue architecture, while ASC alone or combined with SCC exacerbated inflammation and depleted hepatic GSH by 71% and 78%, respectively, relative to BaCl2-exposed controls. Collectively, these results highlight a differential, organ-specific response to BaCl2-induced oxidative stress and the therapeutic potential of SCC and ASC. SCC emerged as a safer and more effective agent, particularly in hepatic protection, while both antioxidants demonstrated neuroprotective effects when used individually or in combination.

Antimicrobial photodynamic inactivation is considered a promising antimicrobial approach that may not develop resistance in the near future. Here, we investigate the influence of the photosensitizer chlorophyllin (CHL) and the cationic permeabilizer polyethylenimine (PEI), exposed to a red light-emitting diode, on the human pathogen Pseudomonas aeruginosa free-living planktonic cells, the sessile biofilm and persister cells. The broth microdilution checkerboard method was used to test antimicrobial susceptibility. As a substrate for biofilms, the Calgary biofilm device was used, and the quantification of the biofilm biomass was carried out using a crystal violet assay. Serine hydroxamate was used for the induction of persisters. Our findings reveal that PEI ameliorates the antimicrobial activity of CHL against P. aeruginosa planktonic and biofilm states, and the concentration required to eradicate the bacteria in the biofilm is more than fourfold that is required to eradicate planktonic cells. Interestingly, the persister cells are more susceptible to CHL/PEI (31.25/100 µg mL−1) than the growing cells by 1.7 ± 0.12 and 0.4 ± 0.1 log10 reduction, respectively, after 15 min of illumination. These data demonstrate that CHL excited with red light together with PEI is promising for the eradication of P. aeruginosa, and the susceptibility of P. aeruginosa to CHL/PEI is influenced by the concentrations and the exposure time.

Background/Objectives: The increasing prevalence of metabolic disorders underscores the need for effective interventions to mitigate environmental stressors such as diesel particulate matter (DPM), a major urban air pollutant. DPM is composed of fine carbonaceous particles that can induce systemic inflammation. This phenomenon results in metabolic dysfunction such as adipocyte hypertrophy, insulin resistance, and mitochondrial impairment in body tissues. Methods: This study investigated the impact of DPM exposure on murine lung, skeletal muscle, and adipose tissues and evaluated the protective effects of supplementation with sodium copper chlorophyllin (SCC). Results: Compared to controls, DPM-exposed mice exhibited significantly elevated oxidative stress markers (* p ≤ 0.05), systemic pro-inflammatory cytokines including TNF-α, MCP-1, IL-6, and IL-1β (* p ≤ 0.05), and adipocyte hypertrophy of both subcutaneous and visceral fat depots, supporting prior findings of DPM-induced metabolic dysfunction. SCC supplementation restored pulmonary ATP levels (* p ≤ 0.05), significantly reduced ROS production in lung and muscle tissue (* p ≤ 0.05), and significantly attenuated DPM-induced inflammatory cytokine secretion (* p ≤ 0.05), while lessening DPM-induced adipocyte hypertrophy. Conclusions: These effects highlight the antioxidant and anti-inflammatory potential of SCC, which likely mitigates systemic metabolic compromise by modulating mitochondrial function and inflammatory pathways. This study further demonstrated that SCC supplementation may be an effective intervention for alleviating the adverse effects of DPM exposure on metabolic and inflammatory compromise. Additional research may clarify a role for SCC in reducing systemic health risks associated with air pollution and offer a foundation for future translational research in human populations exposed to environmental pollutants.

A growing amount of experimental evidence has proven that the application of gold nanorods (AuNRs) in photodynamic therapy (PDT) can significantly enhance its therapeutic efficacy. The aim of this study was to establish a protocol for investigating the effect of gold nanorods loaded with the photosensitizer chlorin e6 (Ce6) on photodynamic therapy in the OVCAR3 human ovarian cancer cell line in vitro and to determine whether the PDT effect was different from that of Ce6 alone. OVCAR3 cells were randomly divided into three groups: the control group, Ce6-PDT group, and AuNRs@SiO2@Ce6-PDT group. Cell viability was measured by MTT assay. The generation of reactive oxygen species (ROS) was measured by a fluorescence microplate reader. Cell apoptosis was detected by flow cytometry. The expression of apoptotic proteins was detected by immunofluorescence and western blotting. The results showed that compared with that of the Ce6-PDT group, the cell viability of the AuNRs@SiO2@Ce6-PDT group was significantly decreased (P < 0.05) in a dose-dependent manner, and ROS production increased significantly (P < 0.05). The flow cytometry results showed that the proportion of apoptotic cells in the AuNRs@SiO2@Ce6-PDT group was significantly higher than that in the Ce6-PDT group (P < 0.05). Immunofluorescence and western blot results showed that the protein expression levels of cleaved caspase-9, cleaved caspase-3, cleaved PARP, and Bax in the AuNRs@SiO2@Ce6-PDT-treated-OVCAR3 cells were higher than those in the Ce6-PDT-treated cells (P < 0.05), and the protein expression levels of caspase-3, caspase-9, PARP, and Bcl-2 were slightly lower than those in the Ce6-PDT group (P < 0.05). In summary, our results show that AuNRs@SiO2@Ce6-PDT has a significantly stronger effect on OVCAR3 cells than the effect of Ce6-PDT alone. The mechanism may be related to the expression of Bcl-2 family and caspase family in the mitochondrial pathway.