In this study, the effect of Phycocyanin (Pc) to ameliorate the cognitive dysfunction in experimental model of Alzheimer's disease (AD) was evaluated. Intracerebroventricular (ICV) induction of Streptozotocin (STZ) (3 mg/kg) was done bilaterally twice in rats on alternative days. Rats were injected with Pc (50, 100 mg/kg; i. p.) for 28 days daily for behavioural and cholinergic activity assessment. As the effect was only significant at 100 mg/kg, later molecular experiments were performed using the same only. STZ induction led to increased activity of hippocampal cholinesterases and BAX and decreased activity of BCL-2 and ChAT. It enhanced TNF-α, and NF-κB in rat's brain and reduced BDNF and IGF-1 levels. Dysfunctional insulin signaling and decreased gene expressions of PI3-K, AKT was also observed. However, Pc treatment significantly prevented STZ-induced increased activity of hippocampal cholinesterases and BAX as well as increased the levels of BCL-2 and ChAT. Neuroinflammation was significantly attenuated and BDNF and IGF-1 levels were upregulated. Further, Pc also alleviated dysfunctional insulin signaling as evidenced by increased gene expression of IRS-1, PI3-K, AKT. In conclusion, our study demonstrated the immense potential of Pc in attenuating STZ-induced cognitive decline and it may be further explored as a therapeutic agent in managing AD.Coronavirus disease 2019 (COVID-19) and previous pandemics have been viewed almost exclusively as virology problems, with toxicology problems mostly being ignored. This perspective is not supported by the evolution of COVID-19, where the impact of real-life exposures to multiple toxic stressors degrading the immune system is followed by the SARS-CoV-2 virus exploiting the degraded immune system to trigger a chain of events ultimately leading to COVID-19. This immune system degradation from multiple toxic stressors (chemical, physical, biological, psychosocial stressors) means that attribution of serious consequences from COVID-19 should be made to the virus-toxic stressors nexus, not to any of the nexus constituents in isolation. The leading toxic stressors (identified in this study as contributing to COVID-19) are pervasive, contributing to myriad chronic diseases as well as immune system degradation. They increase the likelihood for comorbidities and mortality associated with COVID-19.  https://www.selleckchem.com/products/apx2009.html  For the short-term, tactical/reactive virology-focused treatments are of higher priority than strategic/proactive toxicology-focused treatments, although both could be implemented in parallel to reinforce each other. However, for long-term pandemic prevention, toxicology-based approaches should be given higher priority than virology-based approaches. Since current COVID-19 treatments globally ignore the toxicology component almost completely, only limited benefits can be expected from these treatments.During the last decade, the neurotoxicity of the trichothecenes T-2 toxin and deoxynivalenol (DON) has been a major concern, and many important findings have been reported on this topic. Through a summary of relevant research reports in recent years, we discuss the potential neurotoxic mechanisms of T-2 toxin and DON. In neuronal cells, T-2 toxin induces mitochondrial dysfunction and oxidative stress through a series of signalling pathways, including Nrf2/HO-1 and p53. This toxin crosses the blood-brain barrier (BBB) by altering permeability and induces oxidative stress responses, including ROS generation, lipid peroxidation, and protein carbonyl formation. Cellular metabolites (for example, HT-2 toxin) further promote neurotoxic effects. The type B trichothecene DON induces neuronal cell apoptosis via the MAPK and mitochondrial apoptosis pathways. This molecule induces inflammation of the central nervous system, increasing the expression of proinflammatory molecules. DON directly affects brain neurons and glial cells after passing through the BBB and affects the vitality and function of astrocytes and microglia. Exposure to trichothecenes alters brain dopamine levels, decreases ganglion area, and further induces brain damage. In this review, we mainly discuss the neurotoxicity of T-2 toxin and DON. However, our main goal was to reveal the potential mechanism(s) and offer new topics, including the potential of hypoxia-inducible factors, immune evasion, and exosomes, for future research in this context. This review should help elucidate the neurotoxic mechanism of trichothecenes and provides some potential inspiration for the follow-up study of neurotoxicity of mycotoxins.Listeria monocytogenes is a well-known pathogen responsible for the severe foodborne disease listeriosis. The control of L. monocytogenes occurrence in seafood products and seafood processing environments is an important challenge for the seafood industry and the public health sector. However, bacteriophage biocontrol shows great potential to be used as safety control measure in seafood. This review provides an update on Listeria-specific bacteriophages, focusing on their application as a safe and natural strategy to prevent L. monocytogenes contamination and growth in seafood products and seafood processing environments. Furthermore, the main properties required from bacteriophages intended to be used as biocontrol tools are summarized and emerging strategies to overcome the current limitations are considered. Also, major aspects relevant for bacteriophage production at industrial scale, their access to the market, as well as the current regulatory status of bacteriophage-based solutions for Listeria biocontrol are discussed.Acrylamide (AA) is one of the important products of the Maillard reaction. AA hepatotoxicity is related to inflammation, which can be indicated by the activation of NLRP3 inflammasome. In this study, AA activated NLRP3 inflammasome and released a large number of inflammatory factors in HepG2 cells. AA induced oxidative stress (OS) and endoplasmic reticulum stress (ERS) responses in HepG2 cells, accompanied by the activation of the MAPK signaling pathway. When HepG2 cells were pretreated with ROS (NAC) and ERS (4-PBA) inhibitors separately, the activation of NLRP3 inflammasome was inhibited. The MAPK signaling pathway was inhibited when OS and ERS were blocked. HepG2 cells pretreated with MAPK selective inhibitors led to the inhibition on the activation of NLRP3 inflammasome. Overall, we consider that AA induces the activation of NLRP3 inflammasome through the OS- and ERS-mediated MAPK signaling pathway in HepG2 cells.