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Results for “Prodigiosin”

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At least 163 records · Page 9Linked to original sources
PubMed2005

Apoptosis-mediated cytotoxicity of prodigiosin-like red pigment produced by gamma-Proteobacterium and its multiple bioactivities.

Recently we discovered a bacterial strain (MS-02-063) that produces large amounts of red pigment (PG-L-1). Among the cell lines tested, U937 cells showed the highest susceptibility to PG-L-1 toxicity. PG-L-1 induced typical apoptotic nuclear morphological changes, and single cell gel electrophoresis revealed that PG-L-1 caused DNA fragmentation in U937 cells. In PG-L-1 treated U937 cells, the acidic compartment such as lysosomes disappeared, suggesting that PG-L-1-induced disorder of intracellular pH compartmentalization might trigger apoptotic signal. Since p38 MAP kinase inhibitor specifically prevented the PG-L-1 mediated cell death, p38 MAP kinase may be involved in the cytotoxic mechanism. In fact, immunoblot analysis of p38 MAP kinase revealed that phosphorylation of p38 MAP kinase occurred in PG-L-1-treated U937 cells. In addition to the activity to induce apoptotic cell death as reported in several PG family members, our chemiluminescence analysis suggested that PG-L-1 inhibited superoxide generation by 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated U937 cells in a dose-dependent manner. Since PG-L-1 had no effect on the chemiluminescence response caused by xanthine oxidase/hypoxanthine system, PG-L-1 acts on the enzyme system responsible for O(2)(-) generation rather than direct scavenging toward O(2)(-). Our results suggest that PG-L-1 causes multiple biochemical effects on the target cells such as increase in pH in acidic intracellular compartment, activation of p38 MAP kinase, inhibition of O(2)(-) generation, and eventually induces apoptotic cell death.

Acridine Orange↗
PubMed1976

[Effect of prodigiosin on the lysozyme activity in melioidosis].

Decreased lysozyme activity was observed under conditions of melioidosis intoxication in rats induced by intraperitoneal administration of an acetone-killed 3-day culture of the bacterial mass of the melioidosis causative agent. When prodigiozan was administered 48 hours by the 4th day which was indicative of prodigiozan activation of the factors of the microbial non-specific resistance.

Animals↗
PubMed1976

[Study of the effect of tetracycline, prodigiosin and their combination on the dynamics of phagocytosis of plague bacteria].

The advantage of the combined use of prodigiozan and tetracycline was observed in tissue culture of peritoneal macrophages of albino mice. Earlier digestion of the intracellular Y. pestis EV by the animal macrophages exposed to prodigiozan and treated with tetracycline was noted. It was shown that the macrophages preserved during several hours of cultivation in vitro their properties acquired in the animal organism under the effect of the substances administered.

Animals↗
PubMed1975

[Prodigiosin in the overall therapy of dysentery and in the prevention of intrahospital viral respiratory infection in children].

Prodigiozan was tested in complex therapy of children with acute dysentery. Comparison of clinical symptoms, specific immunogenesis and child sanation periods from Shigella in the child groups treated (80) and non-treated (74) with prodigiozan showed that prodigiozan lowered the rate of intrahospital acute respiratory virus infection, provided more favourable dysentery progression, more tensed specific immunity and the patient clearance from Shigella.

Acute Disease↗