Brown pigmentation (lipofuscinosis) of canine intestinal muscularis

Abstract

Day, L. E. (Chas. Pfizer & Co., Inc., Groton, Conn.). Tetracycline inhibition of cell-free protein synthesis. II. Effect of the binding of tetracycline to the components of the system. J. Bacteriol. 92:197-203. 1966.-When tetracycline, an inhibitor of cell-free protein synthesis, was preincubated with each component of the Escherichia coli cell-free system, i.e., ribosomes, soluble ribonucleic acid (sRNA), polyuridylic acid (poly U), and S-100 (supernatant enzymes), only the ribosomal-bound antibiotic was inhibitory to the cell-free assay. Experiments designed to further localize the site of inhibition to either the 50S (Svedberg) or the 30S ribosomal subunit were not conclusive. Tritiated tetracycline (7-H(3)-tetracycline) was bound to isolated 50S ribosomes, and these were recombined with 30S subunits to form 70S ribosomes. When these ribosomes were dissociated and the subunits reisolated, the antibiotic was found with both the 50S and the 30S particles. The same results were observed when the tetracycline was initially bound to the 30S subunit.

Reduction of translating ribosomes enables Escherichia coli to maintain elongation rates during slow growth

“…Towards this end, we characterized the effect of four other protein synthesis inhibitors, tetracycline (Tet), erythromycin (Ery), fusidic acid (FA), and Mupirocin (Mup). Tet inhibits translational elongation by binding tightly to 30S ribosome subunit 23,24 . Erythromycin binds to the 50S subunit of ribosome with a comparably low k off as Cm does (0.15 min −1 ) 25 .…”

Mechanisms of action of systemic antibiotics used in periodontal treatment and mechanisms of bacterial resistance to these drugs

“…They inhibit bacterial protein synthesis by binding to the 30S bacterial ribosome and preventing access of aminoacyl tRNA to the acceptor (A) site on the mRNA-ribosome complex 90,148 . This interrupts the formation of the initiation complex required for amino acid protein synthesis 29 . Tetracyclines can also cause alterations in the cytoplasmic membrane leading to leakage of nucleotides and other compounds from the bacterial cell 109 .…”

Splenic lipofuscinosis in mice

“…Deposition of lipofuscin has been described in a wide variety of other tissues and mammalian species in both normal and pathological states (Trautwein; Cordes and Mosher, 1966) but its restricted distribution and accumulation in such quantities within the spleen has not been previously described in mice or in other experimental animals.…”

“…One aetiological factor thought to be associated with lipofuscin deposition is alphatocopherol (Vitamin E) deficiency (Reddy et al,, 1973). This substance is thought to act as an antioxidant and prevents degeneration of microsomes and mitochondria (Cordes and Mosher;Tappel and Zalkin, 1960). Its deficiency is usually associated with long-standing malabsorption of the other fat soluble vitamins (Wolman) and also subfertility (Draper et al, 1964), but necropsy examination of the animals' intestinal tract and other organs failed to show the presence of any malabsorption or deficiency state and features of gonadal malfunction were not observed in these animals.…”

“…Occasionally, extrinsic toxic factors are also known to cause intracellular accumulation of lipofuscin such as in the case of benzanthracane purgatives in the human colon (Cordes and Mosher;Ghadially and Parry, 1966;Ghadially 1975), prolonged analgesic medication in hepatic and renal lipofuscinosis (Wolman), acetanilide feeding in general lipofuscinosis (Strehler, 1962) and locally after topical application of polyene antibiotics such as Nystatin (Weissman, 1969). No drugs were administered to any of the animals and the random distribution of this phenomenon in animals maintained under similar conditions and also in animals from different units militates somewhat against this being the explanation for the condition.…”