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[
Nematologica,
1979]
Electron microscopy of Caenorhabditis elegans fixed in an aqueous solution of osmium tetroxide mixed with potassium pyroantimonate, silver lactate or lead nitrate revealed the following. Calcium is localised in the median and basal layers of the cuticle, in the myofibrils of the body wall muscle, in mitochondria, and in intestinal cytosomes. Chloride ions are localised in the cortical zone of the cuticle along the apical membrane infoldings of the hypodermal cells and in the ground substance of the cytoplasm and vesicles of intestinal cells. Orthophosphate ions are localised in nucleoli and heterochromatin, in cytosomes of the intestinal cells, in foldings of the external membranes of the hypodermis, and in the intracristal space of mitochondria. Orthophosphates and/or sulphates surround the microvilli of intestinal cells. The results suggest that chloride ion regulation may occur in the hypodermal cells and intestinal cells rather than in the excretory tubules of C. elegans.
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[
Canadian Journal of Zoology,
1979]
Examination of the ultrastructure of the dauer larva of Caenorhabditis elegans showed that cells in the lateral cord and body wall muscle had irregular profiles, few Golgi bodies, and cisternae of endoplasmic reticulum, but they contained abundant lipid and glycogen. These cells and the esophageal cells had mitochondria in the condensed conformation. The intestinal lumen was small and the brush border was so compact that individual microvilli were difficult to discern. Intestinal cells had cytosomes with irregular profiles and unhomogeneous matrices. The striated layer was absent from the cuticle covering the lips and papillae. These ultrastructural features are correlated with the dauer larva's low metabolic rate, its resistance to toxic chemicals and to adverse environmental conditions, and its ability to detect food and to feed soon after exposure to a hospitable environment.
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[
Environ Res,
1979]
The effect of cadmium on the fecundity, growth, and fine structure of the free-living nematode Caenorhabditis elegans was studied. High concentrations of cadmium significantly decreased the fecundity and growth of these organisms. Electron microscopy showed that cadmium modifies the structure of the mitochondria in the esophagus and intestine, causes the formation of inclusion bodies in the nucleus of esophageal cells, and alters the morphology of cytosomes in the intestinal cells. The results suggest that the decreased fecundity and growth of cadmium-exposed C. elegans may be due to cadmium interfering with nutrient uptake or assimilation or both.
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[
Can J Zool,
1978]
The fine structure of the basal zone of the cuticle of the dauerlarva of Caenorhabditis elegans was examined in order to help resolve controversies regarding its structure. The results show that the striated layer in the basal zone consists of two sets of laminae oriented at right angles to each other. One set of laminae consists of longitudinally oriented, alternately thick and thin, osmiophilic strips with the distance between similar strips measuring 19 nm. The other set of laminae consists only of thick strips spaced about 14.5 nm apart which are oriented circumferentially about the larva. It is speculated that the striated layer of the basal zone of the cuticle consists of blocks of protein separated by this apparent network of interconnecting osmiophilic laminae.
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[
Ecotoxicol Environ Saf,
1982]
Mercury toxicity in Caenorhabditis elegans showed as lesions in esophageal muscles and intestinal cells and consisted of degradation of the cytoplasm and the formation of irregularly shaped cytosomes. Specimens intoxicated with silver showed changed cytosomes with a spongy matrix in the intestinal cells and ruffled membranes on the mitochondria of hypodermal cells. General ultrastructural responses reflecting a distress syndrome common to several heavy metals were also noted. The results are discussed with reference to the concept of using free-living nematodes to assist in the diagnosis of the causative toxic heavy metal in a complex.
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Relini A, Tortora P, Gatta E, De Gioia L, Airoldi C, Natalello A, Vertemara J, Visentin C, Penco A, Pellistri F, Regonesi ME, Bonanomi M
[
Hum Mol Genet,
2017]
The protein ataxin-3 (ATX3) triggers an amyloid-related neurodegenerative disease when its polyglutamine stretch is expanded beyond a critical threshold. We formerly demonstrated that the polyphenol epigallocatechin-3-gallate (EGCG) could redirect amyloid aggregation of a full-length, expanded ATX3 (ATX3-Q55) towards non-toxic, soluble, SDS-resistant aggregates. Here, we have characterized other related phenol compounds, although smaller in size, i.e., (-)-epigallocatechin gallate (EGC), and gallic acid (GA). We analyzed the aggregation pattern of ATX3-Q55 and of the N-terminal globular Josephin domain (JD) by assessing the time course of the soluble protein, as well its structural features by FTIR and AFM, in the presence and the absence of the mentioned compounds. All of them redirected the aggregation pattern towards soluble, SDS-resistant aggregates. They also prevented the appearance of ordered side-chain hydrogen bonding in ATX3-Q55, which is the hallmark of polyQ-related amyloids. Molecular docking analyses on the JD highlighted three interacting regions, including the central, aggregation-prone one. All three compounds bound to each of them, although with different patterns. This might account for their capability to prevent amyloidogenesis. Saturation transfer difference NMR experiments also confirmed EGCG and EGC binding to monomeric JD. ATX3-Q55 pre-incubation with any of the three compound prevented its calcium-influx-mediated cytotoxicity towards neural cells. Finally, all the phenols significantly reduced toxicity in a transgenic Caenorhabditis elegans strain expressing an expanded ATX3. Overall, our results show that the three polyphenols act in a substantially similar manner. GA, however, might be more suitable for antiamyloid treatments due to its simpler structure and higher chemical stability.