Deep sea mining concerns the extraction of poly-metallic nodules, cobalt-rich crusts and sulphide deposits from the ocean floor. The exploitation of these resources will result in adverse ecological effects arising from the direct removal of the substrate and, potentially, from the formation of sediment plumes that could result in deposition of fine sediment on sensitive species or entrainment of sediment, chemicals and nutrients into over-lying waters. Hence, identifying the behaviour of deep-sea sediment plumes is important in designing mining operations that are ecologically acceptable. Here, we present the results of novel in situ deep sea plume experiments undertaken on the Tropic seamount, 300 nautical miles SSW of the Canary Islands. These plume experiments were accompanied by hydrographic and oceanographic field surveys and supported by detailed numerical modelling and high resolution video settling velocity measurements of the in situ sediment undertaken in the laboratory. The plume experiments involved the controlled formation of benthic sediment plumes and measurement of the plume sediment concentration at a specially designed lander placed at set distances from the plume origin. The experiments were used as the basis for validation of a numerical dispersion model, which was then used to predict the dispersion of plumes generated by full-scale mining. The results highlight that the extent of dispersion of benthic sediment plumes, resulting from mining operations, is significantly reduced by the effects of flocculation, background turbidity and internal tides. These considerations must be taken into account when evaluating the impact and extent of benthic sediment plumes.

The deep-sea is rich in mineral resources, and deep-sea polymetallic nodules are considered to be the most likely resource for commercial exploitation. Since the discovery of polymetallic nodules by mankind, researchers around the world have made long and arduous explorations in the exploitation of deep-sea polymetallic nodules and have proposed various mining methods, such as the dragging bucket type, the continuous bucket rope type, the automatic shuttle boat type, and the pipeline -lifting type, and have carried out technical verification accordingly. In the collection of seabed polymetallic nodules, the development and testing of towed type, spiral-driven type, crawler self-propelled type, and suspended type technologies have been carried out, basically realizing the mining technology verification of seabed polymetallic nodules and providing technical support for commercial development. However, according to the demand for commercial development, there are still many technical difficulties in polymetallic nodule-collecting technology, and more focus needs to be placed on the efficiency, environmental protection, intelligence, safety, and reliability of the collecting system in the future. This paper compares the existing progress in collection technology and equipment, and provides ideas and references for the research and development of deep-sea polymetallic nodule-mining technology and equipment.

Manganese (II) chloride tetrahydrate was investigated in Swiss mice for maternal and developmental toxicity after subcutaneous (s.c.) exposure to doses of 0, 2, 4, 8 and 16 mg/kg per day from gestation day 6 through 15. Females were sacrificed on gestation day 18, and fetuses were examined for external, visceral, and skeletal abnormalities. Maternal toxicity included significant reductions in weight gain and food consumption at 8 and 16 mg/kg/day, as well as several treatment-related deaths in the high dose-group. There were no treatment-related effects on the number of total implants, early resorptions, dead fetuses or sex ratio, whereas a significant increase in the number of late resorptions was found in the 4, 8, and 16 mg/kg/day groups. Fetotoxicity, consisting primarily of reduced fetal body weight and an increased incidence of morphological defects was also observed at 8 and 16 mg/kg/day. There were no differences between control and manganese-treated groups in the incidence of individual or total malformations. The no observable adverse effect level (NOAEL) for maternal toxicity of MnCl2 x 4H(2)0 in mice was 4 mg/kg/day, while the NOAEL for embryo/fetal toxicity was 2 mg/kg/day.

Manganese is embryotoxic and fetotoxic in mammals. The aim of this study was to determine whether the day of exposure would modify the developmental toxicity of manganese (II). Pregnant Swiss mice were given single sc doses of 50 mg manganese chloride tetrahydrate/kg on day 9, 10, 11 or 12 of gestation. No maternal deaths, abortions or early deliveries were observed. Dams were killed on gestational day 18 and the uterine contents examined. Embryotoxicity, evidenced by significant increases in number of late resorptions and in percentage of postimplantation loss, was especially relevant in groups dosed on gestational days 9 or 10. Fetotoxicity (reduced fetal body weight and increased incidence of skeletal defects) was also especially remarkable from doses on days 9 or 10 of gestation. However, no teratogenic effects were noted in any group. Although mouse conceptus are adversely affected by sc exposure to manganese on any of the gestational days 9-12, days 9 and 10 of gestation are the most sensitive for manganese-induced embryo/fetal toxicity in mice.

The primary influencer of aquaculture quality in Amphioctopus fangsiao is pathogen infection. Both lipopolysaccharides (LPS) and polyinosinic:polycytidylic acid (Poly I:C) are recognized by the pattern recognition receptor (PRR) within immune cells, a system that frequently serves to emulate pathogen invasion. Hemolymph, which functions as a transport mechanism for immune cells, offers vital transcriptome information when A. fangsiao is exposed to pathogens, thereby contributing to our comprehension of the species’ immune biological mechanisms. In this study, we conducted analyses of transcript profiles under the influence of LPS and Poly I:C within a 24 h period. Concurrently, we developed a Weighted Gene Co-expression Network Analysis (WGCNA) to identify key modules and genes. Further, we carried out Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to investigate the primary modular functions. Co-expression network analyses unveiled a series of immune response processes following pathogen stress, identifying several key modules and hub genes, including PKMYT1 and NAMPT. The invaluable genetic resources provided by our results aid our understanding of the immune response in A. fangsiao hemolymph and will further our exploration of the molecular mechanisms of pathogen infection in mollusks.

A common method for calculating results from qPCR experiments is the comparative Ct method, also called the 2-ΔΔCt method. However, several assumptions are included in the 2-ΔΔCt method and standard statistical analyses are not directly applicable. Here, we describe a different method, the X0 method, for result calculations and statistical analysis from qPCR experiments. The X0 method differs from the 2-ΔΔCt method by introducing a conversion of the exponentially related Ct values into linearly related X0 values, which represent the amount of starting material in a qPCR experiment. Results calculated by the X0 method are illustrated for qPCR experiments with technical and biological replicates, including procedures to calculate standard deviations. Incorporation of primer efficiencies in calculations by the X0 method is also described. Altogether, the X0 method constitutes a very simple and accurate alternative to the 2-ΔΔCt method for result calculations from qPCR data.

Manganese (Mn), primarily acquired through diet, is required for brain function and development. Epidemiological studies have found an association between both low and high levels of Mn and impaired neurodevelopment in children. Recent genetic studies have revealed that patients with congenital Mn deficiency display severe psychomotor disability and cerebral and cerebellar atrophy. Although the impact of Mn on gene expression is beginning to be appreciated, Mn-dependent gene expression remains to be explored in vertebrate animals. The goal of this study was to use a mouse model to define the impact of a low-Mn diet on brain metal levels and gene expression. We interrogated gene expression changes in the Mn-deficient mouse brain at the genome-wide scale by RNA-seq analysis of the cerebellum of mice fed low or normal Mn diets. A total of 137 genes were differentially expressed in Mn-deficient cerebellums compared with Mn-adequate cerebellums (Padj < 0.05). Mn-deficient mice displayed downregulation of key pathways involved with “focal adhesion,” “neuroactive ligand-receptor interaction,” and “cytokine-cytokine receptor interaction” and upregulation of “herpes simplex virus 1 infection,” “spliceosome,” and “FoxO signaling pathway.” Reactome pathway analysis identified upregulation of the splicing-related pathways and transcription-related pathways, as well as downregulation of “metabolism of carbohydrate,” and “extracellular matrix organization,” and “fatty acid metabolism” reactomes. The recurrent identifications of splicing-related pathways suggest that Mn deficiency leads to upregulation of splicing machineries and downregulation of diverse biological pathways.

Manganese (Mn) is an essential trace element, but insufficient or excessive bodily amounts can induce neurotoxicity. Mn can directly increase neuronal insulin and activate insulin-like growth factor (IGF) receptors. As an important cofactor, Mn regulates signaling pathways involved in various enzymes. The IGF signaling pathway plays a protective role in the neurotoxicity of Mn, reducing apoptosis in neurons and motor deficits by regulating its downstream protein kinase B (Akt), mitogen-activated protein kinase (MAPK), and mammalian target of rapamycin (mTOR). In recent years, some new mechanisms related to neuroinflammation have been shown to also play an important role in Mn-induced neurotoxicity. For example, DNA-sensing receptor cyclic GMP–AMP synthase (cCAS) and its downstream signal efficient interferon gene stimulator (STING), NOD-like receptor family pyrin domain containing 3(NLRP3)-pro-caspase1, cleaves to the active form capase1 (CASP1), nuclear factor κB (NF-κB), sirtuin (SIRT), and Janus kinase (JAK) and signal transducers and activators of the transcription (STAT) signaling pathway. Moreover, autophagy, as an important downstream protein degradation pathway, determines the fate of neurons and is regulated by these upstream signals. Interestingly, the role of autophagy in Mn-induced neurotoxicity is bidirectional. This review summarizes the molecular signaling pathways of Mn-induced neurotoxicity, providing insight for further understanding of the mechanisms of Mn.

Here, we have compared the behavioral neurotoxicity of a manganese nanoformulation (citrate functionalized MnO nanoparticles; C-MnO NPs) with that of the well-known neurotoxicant, ionic Mn, in an animal model. We found that mice administered with C-MnO NPs showed no signs of a neurobehavioral disorder, but the NPs instead ameliorated Mn-induced neurotoxicity (Parkinson's-like syndrome) through the chelation of excess Mn ions and subsequent reduction of oxidative damage.

Manganese (Mn) is an essential ubiquitous transition metal and, when occupationally or environmentally overexposed, a well-known risk factor for several neurological pathologies. However, the molecular mechanisms underlying Mn-induced neurotoxicity are largely unknown. In this study, addressing RNA-Seq analysis, bioavailability and survival assays, key pathways of transcriptional responses to Mn overexposure were investigated in the model organism Caenorhabditis elegans (C. elegans), providing insights into the Mn-induced cellular stress and damage response. Comparative transcriptome analyses identified a large number of differentially expressed genes (DEGs) in nematodes exposed to MnCl2, and functional annotation suggested oxidative nucleotide damage, unfolded protein response and innate immunity as major damage response pathways. Additionally, a time-dependent increase in the transcriptional response after MnCl2 exposure was identified by means of increased numbers of DEGs, indicating a time-dependent response and activation of the stress responses in Mn neurotoxicity. The data provided here represent a powerful transcriptomic resource in the field of Mn toxicity, and therefore, this study provides a useful basis for further planning of targeted mechanistic studies of Mn-induced neurotoxicity that are urgently needed in the face of increasing industrially caused environmental pollution with Mn.

Manganese (Mn) is an essential trace element due to its participation in many physiological processes. However, overexposure to this metal leads to a neurological disorder known as Manganism whose clinical manifestations and molecular mechanisms resemble Parkinson's disease. Several lines of evidence implicate astrocytes as an early target of Mn neurotoxicity being the mitochondria the most affected organelles. The aim of this study was to investigate the possible mitochondrial dynamics alterations in Mn-exposed human astrocytes. Therefore, we employed Gli36 cells which express the astrocytic markers GFAP and S100B. We demonstrated that Mn triggers the mitochondrial apoptotic pathway revealed by increased Bax/Bcl-2 ratio, by the loss of mitochondrial membrane potential and by caspase-9 activation. This apoptotic program may be in turn responsible of caspase-3/7 activation, PARP-1 cleavage, chromatin condensation and fragmentation. In addition, we determined that Mn induces deregulation in mitochondria-shaping proteins (Opa-1, Mfn-2 and Drp-1) expression levels in parallel with the disruption of the mitochondrial network toward to an exacerbated fragmentation. Since mitochondrial dynamics is altered in several neurodegenerative diseases, these proteins could become future targets to be considered in Manganism treatment. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Exosomes containing the adaptor ASC spread NLRP3 inflammasome activation between cells after manganese exposure.