Transformative and sustainable insights of agricultural waste-based adsorbents for water defluoridation: Biosorption dynamics, economic viability, and spent adsorbent management.

With the progression of civilization, the harmony within nature has been disrupted, giving rise to various ecocidal activities that are evident in every spheres of the earth. These activities have had a profound and far-reaching impact on global health. One significant example of this is the presence of fluoride in groundwater exceeding acceptable limits, resulting in the widespread occurrence of "Fluorosis" worldwide. It is imperative to mitigate the concentration of fluoride in drinking water to meet safety standards. While various defluoridation techniques exist, they often have drawbacks. Biosorption, being a simple, affordable and eco-friendly method, has gained preference for defluoridation. However, its limited commercialization underscores the pressing need for further research in this domain. This comprehensive review article offers a thorough examination of the defluoridation potential of agro-based adsorbents, encompassing their specific chemical compositions and preparation methods. The review presents an in-depth discussion of the factors influencing fluoride biosorption and conducts a detailed exploration of adsorption isotherm and adsorption kinetic models to gain a comprehensive understanding of the nature of the adsorption process. Furthermore, it evaluates the commercial viability through an assessment of regeneration potential and a cost analysis of these agro-adsorbents, with the aim of facilitating the scalability of the defluoridation process. The elucidation of the adsorption mechanism and recommendations for overcoming challenges in large-scale implementation offer a comprehensive outlook on this eco-friendly and sustainable approach to fluoride removal. In summary, this review article equips readers with a lucid understanding of agro-adsorbents, elucidates their ideal conditions for improved performance, offers a more profound insight into the fluoride biosorption mechanism, and introduces the concept of effective spent adsorbent management.

Photodynamic impact of curcumin enhanced silver functionalized graphene nanocomposites on Candida virulence.

Candida species are escalating resistance to conventional antifungal treatments, intensifying their virulence, and obstructing the effectiveness of antifungal medications. Addressing this challenge is essential for effectively managing Candida infections. The overarching objective is to advance the development of more efficient and precise therapies tailored to counter Candida infections. This study focuses on developing antifungal combined drugs using curcumin-enhanced silver-functionalized graphene nanocomposites (Cur-AgrGO) to effectively target key virulence factors of C. albicans, C. tropicalis, and C. glabrata (Candida spp.). The green reduction of graphene oxide (GO) using bioentities and active molecules makes this approach cost-effective and environmentally friendly. The nanocomposites were characterized using various techniques. Combining Cur-AgrGO with photodynamic therapy (PDT) demonstrated effective antifungal and antibiofilm activity with delayed growth and metabolism. The nanocomposites effectively suppressed hyphal transition and reduced key virulence factors, including proteinases, phospholipases, ergosterol levels, and cell membrane integrity. The findings suggest that Cur-AgrGO + PDT has potential as a treatment option for Candida infections. This innovative approach holds promise for treating Candida infections.

Insight interactions of engineered nanoparticles with aquatic higher plants for phytoaccumulation, phytotoxicity, and phytoremediation applications: A review.

With the growing age of human civilization, industrialization has paced up equally which is followed by the innovation of newer concepts of science and technology. One such example is the invention of engineered nanoparticles and their flagrant use in widespread applications. While ENPs serve their intended purposes, they also disrupt the ecological balance by contaminating pristine aquatic ecosystems. This review encompasses a comprehensive discussion about the potent toxicity of ENPs on aquatic ecosystems, with a particular focus on their impact on aquatic higher plants. The discussion extends to elucidating the fate of ENPs upon release into aquatic environments, covering aspects ranging from morphological and physiological effects to molecular-level phytotoxicity. Furthermore, this level of toxicity has been correlated with the determination of competent plants for the phytoremediation process towards the mitigation of this ecological stress. However, this review further illustrates the path of future research which is yet to be explored. Determination of the genotoxicity level of aquatic higher plants could explain the entire process comprehensively. Moreover, to make it suitable to be used in natural ecosystems phytoremediation potential of co-existing plant species along with the presence of different ENPs need to be evaluated. This literature will undoubtedly offer readers a comprehensive understanding of the stress induced by the irresponsible release of engineered nanoparticles (ENP) into aquatic environments, along with insights into the resilience characteristics of these pristine ecosystems.

Quercetin binding accelerates prion fibrillation into proteinase sensitive and loosely structured amyloids.

Amyloidoses are caused by the deposition of amyloid fibrils ascribed to protein misfolding. In this study, we examined the antiamyloidogenic and antioxidative activities of quercetin, a plant flavonol from the flavonoid group of polyphenols, on mouse prion protein (moPrP) with biophysical approaches. As the results show, quercetin binds to the C-terminal region of moPrP, and quercetin binding does not affect the structure of moPrP. However, quercetin binding accelerates moPrP fibrillation and changes the structure of moPrP fibrils. Unlike typical prion fibrils, quercetin-bound fibrils are sensitive to proteinase K and are loosely structured. Moreover, due to high antioxidant activity of flavonoid, quercetin-bound fibrils lack imbalance of free radicals and, therefore, they are nontoxic towards neuroblastoma cells. The quercetin shows its uniqueness from typical antiamyloidogenic drugs which either suppress the development of amyloid or eliminate formed amyloids. Quercetin binding converts moPrP into protease-sensitive and non-cytotoxic fibrils. This work provides a powerful resolution in the advancement of antiamyloidogenic treatment.

Combination of structure-based virtual screening, molecular docking and molecular dynamics approaches for the discovery of anti-prion fibril flavonoids.

Prion diseases are a group of rare neurodegenerative diseases caused by the structural conversion of cellular prion into Scrapie prion resulting aggregated fibrils. Therapy of prion diseases has been developed for several decades, especially drug designs based on the structure of prion monomers. Unfortunately, none of the designed anti-prion drugs function well clinically. To fight against prion fibrils, a drug design based on the precise structure of mammalian prion fibrils is highly required. Fortunately, based on the advantage of newly advanced cryo-electron microscopy (cryo-EM) in the deconvolution of large complexes, three prion fibril structures were resolved in the last 2 years. Based on the cryo-EM solved prion fibril structures, we are able to find some molecules fighting against prion fibrils. Quercetin, one flavonoid molecule in the polyphenol group, has been found to disaggregate the prion fibrils in vitro. In this study, we performed the molecular docking and molecular dynamics simulation on quercetin-like molecules possessing pharmacological properties to evaluate the anti-prion ability of tested molecules. As a result, four quercetin-like molecules interact with prion fibril and decrease the ß-strand content by converting some ß-strands into loop and helical structures to disintegrate the existing fibril structure. The results of this study are significant in the treatment of prion diseases, and the approaches used in this study are applicable to other amyloid diseases.

The Effect of Octapeptide Repeats on Prion Folding and Misfolding.

Misfolding of prion protein (PrP) into amyloid aggregates is the central feature of prion diseases. PrP has an amyloidogenic C-terminal domain with three α-helices and a flexible tail in the N-terminal domain in which multiple octapeptide repeats are present in most mammals. The role of the octapeptides in prion diseases has previously been underestimated because the octapeptides are not located in the amyloidogenic domain. Correlation between the number of octapeptide repeats and age of onset suggests the critical role of octapeptide repeats in prion diseases. In this study, we have investigated four PrP variants without any octapeptides and with 1, 5 and 8 octapeptide repeats. From the comparison of the protein structure and the thermal stability of these proteins, as well as the characterization of amyloids converted from these PrP variants, we found that octapeptide repeats affect both folding and misfolding of PrP creating amyloid fibrils with distinct structures. Deletion of octapeptides forms fewer twisted fibrils and weakens the cytotoxicity. Insertion of octapeptides enhances the formation of typical silk-like fibrils but it does not increase the cytotoxicity. There might be some threshold effect and increasing the number of peptides beyond a certain limit has no further effect on the cell viability, though the reasons are unclear at this stage. Overall, the results of this study elucidate the molecular mechanism of octapeptides at the onset of prion diseases.

Design and synthesis of 4-anilinoquinazolines as Raf kinase inhibitors. Part 1. Selective B-Raf/B-RafV600E and potent EGFR/VEGFR2 inhibitory 4-(3-hydroxyanilino)-6-(1H-1,2,3-triazol-4-yl)quinazolines.

This paper presents the design and synthesis of 4-(3-hydroxyanilino)-6-(1H-1,2,3-triazol-4-yl)quinazolines of scaffold 9 as selective B-Raf/B-RafV600E and potent EGFR/VEGFR2 kinase inhibitors. Total 14 compounds of scaffold 9 having different side chains at the triazolyl group with/without fluoro substituents at the anilino group were synthesized and investigated. Among them, 9m with a 2-carbamoylethyl side chain and C-4'/C-6' difluoro substituents was the most potent, which selectively inhibited B-Raf (IC50: 57 nM) and B-RafV600E (IC50: 51 nM) over C-Raf (IC50: 1.0 µM). Compound 9m also actively inhibited EGFR (IC50: 73 nM) and VEGFR2 (IC50: 7.0 nM) but not EGFRT790M and PDGFR-ß (IC50: >10 µM). Despite having good potency for B-Raf and B-RafV600E in the enzymatic assays, 9m was less active to inhibit melanoma A375 cells which proliferate due to constitutively activated B-Raf600E. The inferior activity of 9m for A375 was similar to that of sorafenib (6), suggesting that 9m might bind to the inactive conformations of B-Raf and B-RafV600E. Docking simulations could thus be performed to reveal the binding poses of 9m in B-Raf, B-RafV600E, and VEGFR2 kinases.

Quercetin Disaggregates Prion Fibrils and Decreases Fibril-Induced Cytotoxicity and Oxidative Stress.

Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases caused by misfolding and aggregation of prion protein (PrP). Previous studies have demonstrated that quercetin can disaggregate some amyloid fibrils, such as amyloid ß peptide (Aß) and α-synuclein. However, the disaggregating ability is unclear in PrP fibrils. In this study, we examined the amyloid fibril-disaggregating activity of quercetin on mouse prion protein (moPrP) and characterized quercetin-bound moPrP fibrils by imaging, proteinase resistance, hemolysis assay, cell viability, and cellular oxidative stress measurements. The results showed that quercetin treatment can disaggregate moPrP fibrils and lead to the formation of the proteinase-sensitive amorphous aggregates. Furthermore, quercetin-bound fibrils can reduce the membrane disruption of erythrocytes. Consequently, quercetin-bound fibrils cause less oxidative stress, and are less cytotoxic to neuroblastoma cells. The role of quercetin is distinct from the typical function of antiamyloidogenic drugs that inhibit the formation of amyloid fibrils. This study provides a solution for the development of antiamyloidogenic therapy.

The Effects of Divalent Cation-Chelated Prion Fibrils on the Immune Response of EOC 13.31 Microglia Cells.

Transmissible spongiform encephalopathies (TSEs) are epidemic neurodegenerative diseases caused by prion proteins; in particular, they are induced by misfolded prion proteins (PrPSc). PrPSc tend to aggregate into insoluble amyloid prion fibrils (fPrPWT), resulting in apoptosis of neuron cells and sequential neurodegeneration. Previous studies indicate that microglia cells play an important role in the innate immune system, and that these cells have good neuroprotection and delay the onset of TSEs. However, microglia can be a double-sided blade. For example, both Cu2+ and Mn2+ can induce microglia activation and secrete many inflammatory cytokines that are fatal to neuron cells. Unfortunately, PrP have cation binding sites at the N-terminus. When PrPSc accumulate during microglial phagocytosis, microglia may change the phenotype to secrete pro-inflammation cytokines, which increases the severity of the disease. Some studies have revealed an increase in the concentration of Mn2+ in the brains of patients. In this study, we treated microglia with fPrPWT and cations and determined IκBα and IL-1ß expression by Western blotting and quantitative polymerase chain reaction. The results showed that Mn-fPrPWT decreased IκBα levels and dramatically increased IL-1ß mRNA expression. In addition, competing binding between Cu2+ and Mn2+ can decrease the effect of Mn-fPrPWT on IκBα and IL-1ß. The effects of divalent cations and fPrPWT in microglia inflammation are also discussed.

Sequential Photodynamic Therapy with Phthalocyanine Encapsulated Chitosan-Tripolyphosphate Nanoparticles and Flucytosine Treatment against Candida tropicalis.

Antibiotic resistance has become a crisis. Candida tropicalis (C. tropicalis) is one of the most highly virulent and drug-resistant pathogens. An alternative antimicrobial therapy to eradicate C. tropicalis effectively, without the risk of developing drug-resistance, is needed. Photodynamic therapy (PDT) is an alternative therapy that does not carry the risk of undesired drug resistance. To target the pathogens and to enhance the cellular penetration of the applied photosensitizer, we fabricated cationic chitosan/tripolyphosphate nanoparticles to encapsulate phthalocyanine. Our strategy promotes the uptake of phthalocyanine four-fold. This enhanced PDT can effectively inhibit planktonic C. tropicalis, such that only ~20% of C. tropicalis in the test survived; but it has a limited ability to inhibit adherent C. tropicalis. Further tests with adherent C. tropicalis indicated that sequential treatment with PDT and flucytosine significantly eliminates pseudohyphae and yeast-like C. tropicalis cells. The cell viability is only ~10% after this sequential treatment. This study provides evidence of an effective therapy against drug resistant C. tropicalis, and this strategy can be potentially applied to other pathogens.

EGFR-targeted photodynamic therapy by curcumin-encapsulated chitosan/TPP nanoparticles.

BACKGROUND: Photodynamic therapy (PDT) is an effective therapy for cancers and is a minimally invasive therapy with low dark toxicity and limited side effects. PDT employs the combination of photosensitizers with a specific light source to produce reactive oxygen species (ROS) to damage tumor cells. METHODS: We fabricated nanoparticles encapsulating curcumin through crosslinking chitosan and tripolyphosphate (TPP). Additionally, the chitosan was conjugated to epidermal growth factor in order to target the epidermal growth factor receptor (EGFR), overexpressed on cancer cells. To investigate PDT using fabricated nanoparticles, we measured cell viabilities and ROS production in relation to EGFR-overexpressing gastric cancer cells and non-cancer gastric cells. RESULTS: The targeting nanoparticles displayed a superior PDT effect in the cancer cell, with a resultant approximately fourfold decrease in the IC50. The PDT mechanism of curcumin-encapsulated nanoparticles is further identified as the generation of 1O2, the major pathway in PDT. CONCLUSION: These curcumin-encapsulated chitosan/TPP nanoparticles are a promising targeted-PDT against EGFR-overexpressing cancers.

An in Vitro Study on the Effect of Combined Treatment with Photodynamic and Chemical Therapies on Candida albicans.

Candida albicans is the most commonly encountered human fungal pathogen, and it is traditionally treated with antimicrobial chemical agents. The antimicrobial effect of these agents is largely weakened by drug resistance and biofilm-associated virulence. Enhancement of the antimicrobial activity of existing agents is needed for effective candidiasis treatment. Our aim was to develop a therapy that combined biofilm disruption with existing antimicrobial agents. Photodynamic therapy (PDT) utilizing curcumin and blue light was tested as an independent therapy and in combination with fluconazole treatment. Viability assays and morphology analysis were used to assess the effectiveness of C. albicans treatment. Results showed that fluconazole treatment decreased the viability of planktonic C. albicans, but the decrease was not as pronounced in adherent C. albicans because its biofilm form was markedly more resistant to the antimicrobiotic. PDT effectively eradicated C. albicans biofilms, and when combined with fluconazole, PDT significantly inhibited C. albicans to a greater extent. This study suggests that the addition of PDT to fluconazole to treat C. albicans infection enhances its effectiveness and can potentially be used clinically.

Thermal lensing effect of CS2 studied with femtosecond laser pulses.

By chopping 820 nm 18 femtosecond (fs)-laser pulses, continuously generated by a self-mode locked Ti:Al2O3 laser at 82 MHz, into trains with both train-width and train-to-train separation considerably longer than the thermal diffusivity time constant τth of CS2, we conducted Z-scan measurements on it at various times relative to the leading pulse of each train (T's). As a result, we observed negative nonlinear refraction strengthening with T within τth and gradually stabilizing with T exceeding τth. We quantitatively explain the experimental results in terms of the thermal lensing effect. In particular, we attribute the heat generation to non-radiative relaxation of libration excited by individual 18 fs-pulses via stimulated Raman scattering. In contrast to the commonly held view of multi-photon excitation, we propose and verify a new heat-generating mechanism for the thermal lensing effect in CS2.

Hypermethylation of the TGF-ß target, ABCA1 is associated with poor prognosis in ovarian cancer patients.

BACKGROUND: The dysregulation of transforming growth factor-ß (TGF-ß) signaling plays a crucial role in ovarian carcinogenesis and in maintaining cancer stem cell properties. Classified as a member of the ATP-binding cassette (ABC) family, ABCA1 was previously identified by methylated DNA immunoprecipitation microarray (mDIP-Chip) to be methylated in ovarian cancer cell lines, A2780 and CP70. By microarray, it was also found to be upregulated in immortalized ovarian surface epithelial (IOSE) cells following TGF-ß treatment. Thus, we hypothesized that ABCA1 may be involved in ovarian cancer and its initiation. RESULTS: We first compared the expression level of ABCA1 in IOSE cells and a panel of ovarian cancer cell lines and found that ABCA1 was expressed in HeyC2, SKOV3, MCP3, and MCP2 ovarian cancer cell lines but downregulated in A2780 and CP70 ovarian cancer cell lines. The reduced expression of ABCA1 in A2780 and CP70 cells was associated with promoter hypermethylation, as demonstrated by bisulfite pyro-sequencing. We also found that knockdown of ABCA1 increased the cholesterol level and promoted cell growth in vitro and in vivo. Further analysis of ABCA1 methylation in 76 ovarian cancer patient samples demonstrated that patients with higher ABCA1 methylation are associated with high stage (P = 0.0131) and grade (P = 0.0137). Kaplan-Meier analysis also found that patients with higher levels of methylation of ABCA1 have shorter overall survival (P = 0.019). Furthermore, tissue microarray using 55 ovarian cancer patient samples revealed that patients with a lower level of ABCA1 expression are associated with shorter progress-free survival (P = 0.038). CONCLUSIONS: ABCA1 may be a tumor suppressor and is hypermethylated in a subset of ovarian cancer patients. Hypermethylation of ABCA1 is associated with poor prognosis in these patients.

FT-IR microspectrometry reveals the variation of membrane polarizability due to epigenomic effect on epithelial ovarian cancer.

Ovarian cancer, as well as other cancers, is primarily caused by methylation at cytosines in CpG islands, but the current marker for ovarian cancer is low in sensitivity and failed in early-stage detection. Fourier transform infrared (FT-IR) spectroscopy is powerful in analysis of functional groups within molecules, and infrared microscopy illustrates the location of specific groups within single cells. In this study, we applied HPLC and FT-IR microspectrometry to study normal epithelial ovarian cell line immortalized ovarian surface epithelium (IOSE), two epithelial ovarian cell lines (A2780 and CP70) with distinct properties, and the effect of a cancer drug 5-aza-2'-deoxycytidine (5-aza) without labeling. Our results reveal that inhibition of methylation on cytosine with 5-aza initiates the protein expression. Furthermore, paraffin-adsorption kinetic study allows us to distinguish hypermethylated and hypomethyated cells, and this assay can be a potential diagnosis method for cancer screening.

Liberation of GPI-anchored prion from phospholipids accelerates amyloidogenic conversion.

Prion diseases or transmissible spongiform encephalopathies are a rare group of fatal neurodegenerative illnesses in humans and animals caused by misfolding of prion protein (PrP). Prion protein is a cell-surface glycosylphosphatidylinositol (GPI)-anchored glycoprotein expressed mostly in the central and peripheral nervous system, and this membrane-bound protein can be cleaved from the cell membranes by phosphoinositide phospholipase C. Numerous studies have investigated GPI-free recombinant PrP, but the role of GPI on misfolding of PrP is not well known. In this study, we synthesized a GPI analog that was covalently linking to a PrP S230C mutant, resulting in S230C-GPI. The structural changes in S230C-GPI upon binding to lipid vesicles composed of mixtures of the zwitterionic lipid (POPC) and the anionic lipid (POPG) were analyzed by circular dichroism spectroscopy, and the amyloid aggregation of S230C-GPI in the liberation from phospholipid vesicles was monitored by proteinase K-digestion assay. Our results indicate that S230C-GPI in the liberation of lipid vesicles has high tendency to misfold into amyloid fibrils, while the membrane-bound S230C-GPI proteins are highly stable and rarely convert into amyloid forms. In addition, the role of cholesterol in S230C-GPI was studied. The effect of GPI, cholesterol and phospholipid vesicles on misfolding of PrP is further discussed.

High-frequency electron nuclear double-resonance spectroscopy studies of the mechanism of proton-coupled electron transfer at the tyrosine-D residue of photosystem II.

The solar water-splitting protein complex, photosystem II, catalyzes one of the most energetically demanding reactions in Nature by using light energy to drive the catalytic oxidation of water. Photosystem II contains two symmetrically placed tyrosine residues, YD and YZ, one on each subunit of the heterodimeric core. The YZ residue is kinetically competent and is proposed to be directly involved in the proton-coupled electron transfer reactions of water oxidation. In contrast, the YD proton-coupled electron transfer redox poises the catalytic tetranuclear manganese cluster and may electrostatically tune the adjacent monomeric redox-active chlorophyll and ß-carotene in the secondary electron transfer pathway of photosystem II. In this study, we apply pulsed high-frequency electron paramagnetic resonance (EPR) and electron nuclear double-resonance (ENDOR) spectroscopy to study the photochemical proton-coupled electron transfer (PCET) intermediates of YD. We detect the "unrelaxed" and "relaxed" photoinduced PCET intermediates of YD using high-frequency EPR spectroscopy and observe an increase of the g anisotropy upon temperature-induced relaxation of the unrelaxed intermediate to the relaxed state as previously observed by Faller et al. [(2002) Biochemistry 41, 12914-12920; (2003) Proc. Natl. Acad. Sci. U.S.A. 100, 8732-8735]. This observation suggests the presence of structural differences between the two intermediates. We probe the possible structural differences by performing high-frequency (2)H ENDOR spectroscopy experiments. On the basis of numerical simulations of the experimental (2)H ENDOR spectra, we confirm that (i) there is a significant change in the H-bond length of the tyrosyl radical in the unrelaxed (1.49 Å) and relaxed (1.75 Å) PCET intermediates. This observation suggests that the D2-His189 residue is deprotonated prior to electron transfer at the YD residue and (ii) there are negligible changes in the conformation of the tyrosyl ring in the unrelaxed and relaxed PCET intermediates of YD.

Areca nut extract induces pyknotic necrosis in serum-starved oral cells via increasing reactive oxygen species and inhibiting GSK3ß: an implication for cytopathic effects in betel quid chewers.

Areca nut has been proven to be correlated with various pathologic alterations in oral cavity. However, the mechanisms for such cytopathic effects are still elusive due mostly to the limitations of cell culture systems. Here we discovered that areca nut extract (ANE) induced production of autophagosome vacuoles in cells cultured with rich medium but induced pyknosis and ballooning, two morphological alterations frequently observed in betel quid chewers, in cells under a serum-free culture condition. Permeability of the serum-starved cells to propidium iodide (PI) confirmed ANE induced novel necrosis with pyknosis (pyknotic necrosis), providing a possible explanation for inflammatory infiltration in chewers' mucosa. In these serum-starved cells, ANE strongly induced reactive oxygen species (ROS), which acted as a key switch for the initiation of pyknotic necrosis. Calcium flux was also involved in the morphological alterations. Besides, inhibition of GSK3ß by SB216763 significantly exacerbated the pyknotic necrosis either induced by ANE or H2O2 in serum-starved cells, suggesting that GSK3ß is a critical regulator for ANE/ROS-mediated pyknotic necrosis. Interestingly, LC3-II transition and PARP cleavage were still detected in the serum-starved cells after ANE treatment, suggesting concurrent activation of apoptotic and autophagic pathways. Finally, insulin could counteract the effect of ANE-induced pyknotic necrosis. Taken together, these data provide a platform for studying ANE-induced cytopathogenesis and the first clinical implication for several pathological alterations, such as ballooning and inflammatory infiltration, in betel quid chewers.

Curcumin reduces amyloid fibrillation of prion protein and decreases reactive oxidative stress.

Misfolding and aggregation into amyloids of the prion protein (PrP) is responsible for the development of fatal transmissible neurodegenerative diseases. Various studies on curcumin demonstrate promise for the prevention of Alzheimer's disease and inhibition of PrPres accumulation. To evaluate the effect of curcumin on amyloid fibrillation of prion protein, we first investigated the effect of curcumin on mouse prion protein (mPrP) in a cell-free system. Curcumin reduced the prion fibril formation significantly. Furthermore, we monitored the change in apoptosis and reactive oxygen species (ROS) level upon curcumin treatment in mouse neuroblastoma cells (N2a). Curcumin effectively rescues the cells from apoptosis and decreases the ROS level caused by subsequent co-incubation with prion amyloid fibrils. The assays in cell-free mPrP and in N2a cells of this work verified the promising effect of curcumin on the prevention of transmissible neurodegenerative diseases.

Formation of amyloid fibrils from ß-amylase.

Fibril formation has been considered a significant feature of amyloid proteins. However, it has been proposed that fibril formation is a common property of many proteins under appropriate conditions. We studied the fibril formation of ß-amylase, a non-amyloid protein rich in α-helical structure, because the secondary structure of ß-amylase is similar to that of prions. With the conditions for the fibril formation of prions, ß-amylase proteins were converted into amyloid fibrils. The features of ß-amylase proteins and fibrils are compared to prion proteins and fibrils. Furthermore, the cause of neurotoxicity in amyloid diseases is discussed.