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Cell structure Rough endoplasmic reticulum

Liver. In humans, chronic Cd exposure does not typically result in hepatotoxicity. In laboratory animals, the liver accumulates the largest concentrations of Cd after acute or chronic exposures. In chronically exposed rats, liver injury occurs prior to renal dysfunction. Chronic Cd effects in the liver include increased plasma activities of alanine and aspartate aminotransferases, structural irregularities in hepatocytes, and decreased microsomal mixed function oxidase and CYP450 activities. Acute exposures in rats result in hepatic necrosis, particularly in parenchymal cells. Additionally, rough endoplasmic reticulum deteriorates, while smooth endoplasmic reticulum proliferates. Mitochondria are also degraded. As is the case with chronic exposure, microsomal mixed function oxidases and CYP450s are inhibited. [Pg.430]

Experiment 5. Observation under transmission electron microscope We compared the TEM ultrastructure of the seed coat and endosperm of control and rue-treated seeds The palisade layer of treated seed appears thicker than in the control (Figs 6A and 7A), while comparison between aleuronic cells of the control and treated cells (Figs. 6B and 7B), reveals that the cells of the control are healthy with some evident organelles such as the nucleus and the rough endoplasmic reticulum and other structures, the plastid, the plasmodesmata, conspicous constrictions, protein bodies and... [Pg.80]

As would be expected of active protein secreting cells, glandular epithelial tissue, the cytokine secreting cells of the immune system and the blood vessel endothelium, have an extensive internal structure consisting of rough endoplasmic reticulum and numerous mitochondria. Peptide hormones, growth factors and cytokines like all proteins are synthesized by DNA transcription and mRNA translation. The primary transcript of the mRNA may code for an inactive prohormone which requires careful proteolysis to produce the active hormone, as for example in the case of insulin. Adrenocorticotropic hormone (ACTH) is particularly interesting in this respect because... [Pg.86]

Intracellular antigens could be modified internal proteins, which are continuously removed by the cell, the structure altered and attached to MHC I. This takes place in the rough endoplasmic reticulum. The protein/pep tide-hapten fragments are then presented to the external surface of the cell membrane as a complex with the MHC I. Then cytotoxic T cells (CD8+) accept the protein/peptide and destroy the cell. This mechanism gives rise to a type IV response. [Pg.254]

The rough endoplasmic reticulum contains ribosomes on the surfaces, a cell structure that will be discussed in the next section. The system formed by endoplasmic reticulum and ribosomes is associated with protein synthesis. The endoplasmic reticulum also participates in lipid biosynthesis. In different types of eukaryotic cells, the endoplasmic reticulum has different forms and functions. In muscle cells, in which Ca2+ stimulates contraction, the endoplasmic reticulum participates in the relaxation process, reabsorbing Ca2+ ions. [Pg.15]

Ribosomes are spherical cell structures enriched with ribonucleoprotein and with a diameter of 15-20 nm. Each ribosome is formed by two subunits of different sizes, only visible through high resolution electron microscopy. Ribosomes connected to the rough endoplasmic reticulum are involved in the biosynthesis of proteins that are temporarily stored or transported to the cell s outer environment. Proteins synthesized by ribosomes connected to membranes accumulate in the cisternae before passage to the plasma membrane for secretion. [Pg.16]

Desmosomes and Filaments. The cohesiveness and internal structure of SC cells are dependent on the structures that are called desmosomes (25, 26, 27). These structures unite SC cells of different layers (Figure 3) and of the same layer (Figures 4 and 5). The sequence of embryonic development is a thickening of opposed cell membranes followed by intercellular disc formation and intracellular formation of the attachment plate (25, 29). This sequence is blocked if normal protein production in rough endoplasmic reticulum is altered by virus activity (28). When complete, the desmosomes of basal cells sprout filaments from their attachment plates (25, 27, 30). These filaments become longer, thicker, and more numerous as cells differentiate and migrate toward the skin surface (31, 32). Filaments arise either from the attachment plate (27) or they form loops that are anchored there (26). The smallest filaments... [Pg.45]

Neurotransmission is based on the secretion of neurotransmitters from secretory vesicles in the presynaptic membrane and the binding of the agonists by receptors on the postsynaptic membrane. The transmitters have to travel only about 20 nm across the synaptic cleft, whereas neurohormones may act on much more distant receptors. The biogenesis of the secretory vesicles and the receptors are intimately connected with the secretory pathway of the eukaryotic cells. In this system a series of membrane-bound structures mediate the transfer of exported proteins from their site of synthesis at the rough endoplasmic reticulum to their site of discharge at the plasma membrane. We will use the chromaffin granules (storage vesicles of the adrenal medulla) as an example for secretory vesicles, and the acetylcholine receptor for receptors of neurotransmitters. [Pg.356]

In most eukaryotic cells two major classes of ribosomes exist attached ribosomes and free ribosomes. The attached ribosomes are bound to an extensive cytoplasmic network of lipoprotein membranes called the endoplasmic reticulum. The rough endoplasmic reticulum consists of bound ribosomes the smooth endoplasmic reticulum is devoid of ribosomes. There is no structural difference between a... [Pg.580]

The ultramicrostructural alterations of the thyroid caused by overdosed iodine included a decrease of microvilli, dilation of rough endoplasmic reticulum, vacuolation of mitochondria, an increase in peroxidates and secondary lyso-somes, an increase in myelin-sheath structures in cytoplasm, and apoptosis and necrosis of thyroid epithelial cells. In contrast to Wistar rats, iodine excess could also cause infiltration of lymphocytes and proliferation of fibrous tissue in NOD. H-2 mice, which showed a positive correlation with the iodine dose. Similar results were found in other susceptible animals (Li et ai, 1993 Bagchi et at, 1995). When human thyroid cells were cultured with excessive iodine in vitro, Many et al. (1992) observed the same phenomenon under the electron microscope, such as dilated mitochondria, rough endoplasmic reticulum, increased secondary lysosomes, apoptosis and necrosis of epithelial cells, and a positive correlation between the ratio of apoptosis and iodine. [Pg.883]

Cyclicine, cyproheptadine and some other structurally related antihistaminics, when administered to rats, provoked a marked degranulation of the pancreatic beta cells together with a dramatic dilatation of the rough endoplasmic reticulum (Hru-BAN et al. 1972, Longnecker et al. 1972, Fischer et al. 1973,1975). In fed, fasting and adrenalectom-ized rats cyproheptadine (10-40 mg/kg) caused a hyperglycaemia and a fall in plasma insulin (Poser et al. 1975). [Pg.288]


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See also in sourсe #XX -- [ Pg.14 , Pg.15 ]




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