Prevention by the MER tubercle bacillus fraction of immunosuppression induced by cancer chemotherapeutic agents

1976 ◽  
Vol 1 (4) ◽  
Author(s):  
Y. Stupp ◽  
R. Saltoun ◽  
D.W. Weiss
Keyword(s):  
Chemotherapeutic Agents ◽  
Tubercle Bacillus

Prostatic Acid Phosphatase (PAP) Differentiated Ultracytochemically from Lysosomal Acid Phosphate in the Rat with a PAP/Specific Substrate, Phosphorylcholine

1975 ◽  
Vol 33 ◽  
pp. 450-451
Author(s):  
W. Allen Shannon ◽  
José A. Serrano ◽  
Hannah L. Wasserkrug ◽  
Anna A. Serrano ◽  
Arnold M. Seligman
Keyword(s):  
Acid Phosphatase ◽  
Phosphate Buffer ◽  
Prostatic Carcinoma ◽  
Prostatic Acid Phosphatase ◽  
Chemotherapeutic Agents ◽  
Specific Substrate ◽  
Acid Phosphate ◽  
Lysosomal Acid ◽  
Design And Synthesis ◽  
New Chemotherapeutic Agents

During the design and synthesis of new chemotherapeutic agents for prostatic carcinoma based on phosphorylated agents which might be enzyme-activated to cytotoxicity, phosphorylcholine, [(CH3)3+NCH2CH2OPO3Ca]Cl-, has been indicated to be a very specific substrate for prostatic acid phosphatase (PAP). This phenomenon has led to the development of specific histochemical and ultracytochemical methods for PAP using modifications of the Gomori lead method for acid phosphatase. Comparative histochemical results in prostate and kidney of the rat have been published earlier with phosphorylcholine (PC) and β-glycerophosphate (βGP). We now report the ultracytochemical results.Minced tissues were fixed in 3% glutaraldehyde-0.1 M phosphate buffered (pH 7.4) for 1.5 hr and rinsed overnight in several changes of 0.05 M phosphate buffer (pH 7.0) containing 7.5% sucrose. Tissues were incubated 30 min to 2 hr in Gomori acid phosphatase medium (2) containing 0.1 M substrate, either PC or βGP.

Activation of cytochrome c to a peroxidase compound I-type intermediate by H2O2: relevance to redox signalling in apoptosis

2004 ◽  
Vol 71 ◽  
pp. 97-106 ◽  
Author(s):  
Mark Burkitt ◽  
Clare Jones ◽  
Andrew Lawrence ◽  
Peter Wardman
Keyword(s):  
Cytochrome C ◽  
Hydroxyl Radical ◽  
Redox Regulation ◽  
Chemotherapeutic Agents ◽  
Tyrosyl Radical ◽  
Compound I ◽  
Definitive Evidence ◽  
Enhanced Production ◽  
Physico Chemical

The release of cytochrome c from mitochondria during apoptosis results in the enhanced production of superoxide radicals, which are converted to H2O2 by Mn-superoxide dismutase. We have been concerned with the role of cytochrome c/H2O2 in the induction of oxidative stress during apoptosis. Our initial studies showed that cytochrome c is a potent catalyst of 2′,7′-dichlorofluorescin oxidation, thereby explaining the increased rate of production of the fluorophore 2′,7′-dichlorofluorescein in apoptotic cells. Although it has been speculated that the oxidizing species may be a ferryl-haem intermediate, no definitive evidence for the formation of such a species has been reported. Alternatively, it is possible that the hydroxyl radical may be generated, as seen in the reaction of certain iron chelates with H2O2. By examining the effects of radical scavengers on 2′,7′-dichlorofluorescin oxidation by cytochrome c/H2O2, together with complementary EPR studies, we have demonstrated that the hydroxyl radical is not generated. Our findings point, instead, to the formation of a peroxidase compound I species, with one oxidizing equivalent present as an oxo-ferryl haem intermediate and the other as the tyrosyl radical identified by Barr and colleagues [Barr, Gunther, Deterding, Tomer and Mason (1996) J. Biol. Chem. 271, 15498-15503]. Studies with spin traps indicated that the oxo-ferryl haem is the active oxidant. These findings provide a physico-chemical basis for the redox changes that occur during apoptosis. Excessive changes (possibly catalysed by cytochrome c) may have implications for the redox regulation of cell death, including the sensitivity of tumour cells to chemotherapeutic agents.

KIDNEY INJURY IN CANCER THERAPY

2018 ◽  
Vol 22 (5) ◽  
pp. 17-24 ◽  
Author(s):  
E. V. Burnasheva ◽  
Y. V. Shatokhin ◽  
I. V. Snezhko ◽  
A. A. Matsuga
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Cancer Therapy ◽  
Cancer Patients ◽  
Cytotoxic Effect ◽  
Tumor Lysis Syndrome ◽  
Kidney Injury ◽  
Chemotherapeutic Agents ◽  
Oxygen Intermediates ◽  
Circulating Blood Volume

Кidney injury is a frequent and significant complication of cancer and cancer therapy. The kidneys are susceptible to injury from malignant infiltration, damage by metabolites of malignant cells, glomerular  injury, nephrotoxic drugs including chemotherapeutic agents. Also  bone marrow transplantation complications, infections with immune  suppression (including septicemia), tumor lysis syndrome should be  taken into account. Chemotherapeutic agents are a common cause  of acute kidney injury but can potentially lead to chronic kidney  disease development in cancer patients. This article summarizes risk  factors of acute kidney injury in cancer patients. Risk factors are  divided into two groups. The systemic are decrease of total  circulating blood volume, infiltration of kidney tissue by tumor cells,  dysproteinemia, electrolyte disturbances. The local (renal) risk  factors are microcirculation disturbances, drugs biotransformation  with formation of reactive oxygen intermediates, high concentration of nephrotoxic agents in proximal tubules and its  sensitivity to ischemia. Drug-related risk factors include: drugs  combination with cytotoxic effect high doses long term use necessity, direct cytotoxic effect of not only chemotherapeutic agents but also its metabolites, mean solubility forming intratubular  precipitates. Early diagnosis, timely prevention and treatment of  these complications provide significantly improve nononcologic results of treatment.

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