bims-metalz Biomed News
on Metabolic causes of Alzheimer’s disease
Issue of 2023–12–31
six papers selected by
Mikaila Chetty, Goa University
  1. Toxicity mechanism of engineered nanomaterials: Focus on mitochondria.
  2. Exploring the environmental factor fulvic acid attenuates the ecotoxicity of graphene oxide under food delivery exposure.
  3. [Environmental pollutants and Alzheimer's disease].
  4. Parental treatment with selenium protects Caenorhabditis elegans and their offspring against the reproductive toxicity of mercury.
  5. Juggling cadmium detoxification and zinc homeostasis: A division of labour between the two C. elegans metallothioneins.
  6. Does Gut Brain Axis has an impact on Parkinson's Disease (PD)?
  1. Environ Pollut. 2023 Dec 26. pii: S0269-7491(23)02233-9. [Epub ahead of print] 123231
    Toxicity mechanism of engineered nanomaterials: Focus on mitochondria.
    Yongshuai Yao, Ting Zhang, Meng Tang.
      With the rapid development of nanotechnology, engineered nanomaterials (ENMs) are widely used in various fields. This has exacerbated the environmental pollution and human exposure of ENMs. The study of toxicity of ENMs and its mechanism has become a hot research topic in recent years. Mitochondrial damage plays an important role in the toxicity of ENMs. This paper reviews the structural damage, dysfunction, and molecular level perturbations caused by different ENMs to mitochondria, including ZnO NPs, Ag NPs, TiO2 NPs, iron oxide NPs, cadmium-based quantum dots, CuO NPs, silica NPs, carbon-based nanomaterials. Among them, mitochondrial quality control plays an important role in mitochondrial damage. We further summarize the cellular level outcomes caused by mitochondrial damage, mainly including, apoptosis, ferroptosis, pyroptosis and inflammation response. In addition, we concluded that reducing mitochondrial damage at source as well as accelerating recovery from mitochondrial damage through ENMs modification and pharmacological intervention are two feasible strategies. This review further provides new insights into the mitochondrial toxicity mechanisms of ENMs and provides a new foothold for predicting human health and environmental risks of ENMs.
    Keywords:  ENMs design strategies; Engineered nanomaterials (ENMs); Ferroptosis; Inflammation; Mitochondrial quality control; Mitochondrial toxicity
    DOI:  https://doi.org/10.1016/j.envpol.2023.123231
  2. Ecotoxicol Environ Saf. 2023 Dec 27. pii: S0147-6513(23)01397-0. [Epub ahead of print]270 115893
    Exploring the environmental factor fulvic acid attenuates the ecotoxicity of graphene oxide under food delivery exposure.
    Xun Luo, Yajun Zhang, Yun Wang, Qianduo Chen, Junfang Tu, Mei He, Jiaming Zhang, Yu Wu.
      There is limited understanding of nanoparticle potential ecotoxicity, particularly regarding the influence of environmental factors that can be transferred through the food chain. Here, we assessed the transfer behavior and the ecotoxicity of commercially manufactured graphene oxide nano-materials (GO, <100 nm) in a food chain perspective spanning from Escherichia coli (E. coli) to Caenorhabditis elegans (C. elegans) under simulated environmental conditions. Our findings revealed that E. coli preyed upon GO, subsequently transferring it to C. elegans, with a discernible distribution of GO observed in the digestive system and reproductive system. Accumulated GO generated serious ecological consequences for the higher level of the food chain (C. elegans). More importantly, GO and the resulting injurious effects of germ cells could be transferred to the next generation, indicating that GO exposure could cause genetic damage across generations. Previous research has demonstrated that GO can induce degradation of both the inner and outer cell membranes of E. coli, which is then transmitted to C. elegans through the food chain. Additionally, fulvic acid (FA) possesses various functional groups that enable interaction with nanomaterials. Our findings indicated that these interactions could mitigate ecotoxicity caused by GO exposure via food delivery, and this approach could be extended to modify GO in a way that significantly reduced its toxic effects without compromising performance. These results highlighted how environmental factors could attenuate ecological risks associated with nanomaterial transmission through the food chain.
    Keywords:  Apoptosis; C. elegans; Ecotoxicity; Food chain; Graphene oxide; Population size
    DOI:  https://doi.org/10.1016/j.ecoenv.2023.115893
  3. Sheng Li Xue Bao. 2023 Dec 25. 75(6): 740-766
    [Environmental pollutants and Alzheimer's disease].
    Bao Guo, Qian Ba.
      Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive impairment. The main hypotheses about the pathogenesis of AD include the hypothesis of β-amyloid protein, the hypothesis of abnormal phosphorylation of Tau protein, and the hypothesis of neuroinflammation. In recent years, environmental pollutants have been considered as an important factor in causing neurological dysfunction. Common environmental pollutants include heavy metals, pesticides, polychlorinated biphenyls, microplastics, and air pollutants, all of which have been proven to have neurotoxicity. In this review, we not only discussed epidemiological and animal experimental studies that link environmental pollution with AD, but also summarized the mechanisms of action of relevant toxins, providing insights for studying the interrelationships between environmental pollutants and AD.
  4. Sci Total Environ. 2023 Dec 21. pii: S0048-9697(23)08091-9. [Epub ahead of print] 169461
    Parental treatment with selenium protects Caenorhabditis elegans and their offspring against the reproductive toxicity of mercury.
    Yanan Zhao, Shenyao Ni, Chengcheng Pei, Lingyan Sun, Lijun Wu, An Xu, Yaguang Nie, Yun Liu.
      Mercury (Hg) is one of the major pollutants in the environment, which requires effective countermeasures to manage its risk to both human health and the ecosystem. The antagonistic effect of selenium (Se) against methyl mercury (MeHg) and HgCl2 was evaluated using parent and offspring Caenorhabditis elegans (C. elegans) in this study. Through designated acute exposure of 24 h, our results showed that both MeHg and HgCl2 induced dose-dependent reproductive toxicity, including increased germ cell apoptosis, decrease in the number of oocytes, brood size, and sperm activation. The increased germ cell apoptosis was even higher in F1 and F2 generations, but returned to control level in F3. Pretreatment of Se significantly suppressed the reproductive toxicity caused by Hg in both parental worms and their offspring, but had little influence on Hg accumulation. The protective role of Se was found closely related to the chemical forms of Hg: mtl-1 and mtl-2 genes participated in reducing the toxicity of HgCl2, while the gst-4 gene was involved in the reduced toxicity of MeHg. The formation of Se-Hg complex and the antioxidant function of Se were considered as possible antagonistic mechanisms. Our data indicated that pretreatment with Se could effectively protect C. elegans and their offspring against the reproductive toxicity of Hg in different chemical forms, which provided a reference for the prevention of Hg poisoning and essential information for better understanding the detoxification potential of Se on heavy metals.
    Keywords:  Caenorhabditis elegans; Mercury; Offspring; Reproductive toxicity; Selenium
    DOI:  https://doi.org/10.1016/j.scitotenv.2023.169461
  5. Chemosphere. 2023 Dec 25. pii: S0045-6535(23)03291-5. [Epub ahead of print] 141021
    Juggling cadmium detoxification and zinc homeostasis: A division of labour between the two C. elegans metallothioneins.
    Yona J Essig, Oksana I Leszczyszyn, Norah Almutairi, Alexandra Harrison-Smith, Alix Blease, Sukaina Zeitoun-Ghandour, Sam M Webb, Claudia A Blindauer, Stephen R Stürzenbaum.
      The chemical properties of toxic cadmium and essential zinc are very similar, and organisms require intricate mechanisms that drive selective handling of metals. Previously regarded as unspecific "metal sponges", metallothioneins (MTLs) are emerging as metal selectivity filters. By utilizing C. elegans mtl-1 and mtl-2 knockout strains, metal accumulation in single worms, single copy fluorescent-tagged transgenes, isoform specific qPCR and lifespan studies it was possible to demonstrate that the handling of cadmium and zinc by the two C. elegans metallothioneins differs fundamentally: the MTL-2 protein can handle both zinc and cadmium, but when it becomes unavailable, either via a knockout or by elevated cadmium exposure, MTL-1 takes over zinc handling, leaving MTL-2 to sequester cadmium. This division of labour is reflected in the folding behaviour of the proteins: MTL-1 folded well in presence of zinc but not cadmium, the reverse was the case for MTL-2. These differences are in part mediated by a zinc-specific mononuclear His3Cys site in the C-terminal insertion of MTL-1; its removal affected the entire C-terminal domain and may shift its metal selectivity towards zinc. Overall, we uncover how metallothionein isoform-specific responses and protein properties allow C. elegans to differentiate between toxic cadmium and essential zinc.
    Keywords:  Cadmium; Caenorhabditis elegans; Detoxification; Metallothionein
    DOI:  https://doi.org/10.1016/j.chemosphere.2023.141021
  6. Ageing Res Rev. 2023 Dec 21. pii: S1568-1637(23)00330-6. [Epub ahead of print] 102171
    Does Gut Brain Axis has an impact on Parkinson's Disease (PD)?
    Ajay Elangovan, Bhawna, Laxmi Kirola, Mahalaxmi Iyer, Priyanka Jeeth, Sakshi Maharaj, Nikki Kumari, Vikas Lakhanpal, Tanja Maria Sheldrick-Michel, K R S Sambasiva Rao, Ssang-Goo Cho, Mukesh Kumar Yadav, Abilash Valsala Gopalakrishnan, Saraboji Kadhirvel, Nachimuthu Senthil Kumar, Balachandar Vellingiri.
      Parkinson's Disease (PD) is becoming a growing global concern by being the second most prevalent disease next to Alzheimer's Disease (AD). Henceforth new exploration is needed in search of new aspects towards the disease mechanism and origin. Evidence from recent studies has clearly stated the role of Gut Microbiota (GM) in the maintenance of the brain and as a root cause of various diseases and disorders including other neurological conditions. In the case of PD, with an unknown etiology, the GM is said to have a larger impact on the disease pathophysiology. Although GM and its metabolites are crucial for maintaining the normal physiology of the host, it is an undeniable fact that there is an influence of GM in the pathophysiology of PD. As such the Enteroendocrine Cells (EECs) in the epithelium of the intestine are one of the significant regulators of the gut-brain axis and act as a communication mediator between the gut and the brain. The communication is established via the molecules of neuroendocrine which are said to have a crucial part in neurological diseases such as AD, PD, and other psychiatry-related disorders. This review is focused on understanding the proper role of GM and EECs in PD. Here, we also focus on some of the metabolites and compounds that can interact with the PD genes causing various dysfunctions in the cell and facilitating the disease conditions using bioinformatical tools. Various mechanisms concerning EECs and PD, their identification, the latest studies, and available current therapies have also been discussed.
    Keywords:  Enteroendocrine Cells (EECs); Gut Microbiota (GM); Gut-brain axis; Neurodegeneration; Parkinson’s Disease (PD)
    DOI:  https://doi.org/10.1016/j.arr.2023.102171
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