Protection of bone marrow progenitor cells by superoxide dismutase

Petkau, A.

doi:10.1007/bf00421047

Cited by 11 publications

(2 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gao et al [72]found that radiation resistance was increased in human glioma cells over expressing SOD1. Similarly, Petkau [73] found that SOD1 activity increased the recovery of hematopoietic myeloid progenitor cell recovery in X-irradiated mice. The mechanisms appears to be a consequence of suppression of superoxide-mediated induction of apoptosis [72].…”

Section: Nrf2 Promotes Repair Of Damaged Dnamentioning

confidence: 94%

Nrf2 promotes survival following exposure to ionizing radiation

Sekhar

Freeman

2015

Free Radical Biology and Medicine

View full text Add to dashboard Cite

NRF2 is a transcription factor that promotes antioxidant and drug-metabolizing gene expression. It also regulates the transcription of genes involved in carbohydrate and lipid metabolism, NADPH regeneration, heme and iron metabolism, as well as proteasome metabolism. Emerging research has identified NRF2 as a critical factor for promoting survival of mammalian cells subjected to ionizing radiation. At a mechanistic level, NRF2 promotes the repair of DNA damage and drives detoxification of superoxide that is generated hours to days after irradiation. This review summarizes research in these areas and discusses targeting of NRF2 in radiation resistant cancer and NRF2’s role in mitigating Acute Radiation Syndrome.

show abstract

Section: Nrf2 Promotes Repair Of Damaged Dnamentioning

confidence: 94%

Nrf2 promotes survival following exposure to ionizing radiation

Sekhar

Freeman

2015

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…However, recent observations suggest that A 0 may also play an important role in the growth and, potentially, leukemogenesis of hematopoietic cells. Subpopulations of myeloid progenitor cells are hypersensitive to superoxide radicals (Petkau, 1988). Clonal growth of hematopoietic cells is enhanced in the presence of anti-oxidant enzymes (Lin and Hsie, 1986).…”

mentioning

confidence: 99%

Active oxygen transforms murine myeloid progenitor cells in vitro

Crawford

Greenberger

1991

Intl Journal of Cancer

View full text Add to dashboard Cite

Active oxygen (AO) is ubiquitous in nature and its many forms can act as natural carcinogens. Their effect on the transformation of a mouse myeloid progenitor cell line was studied using anchorage-independent colony formation in methylcellulose as the primary assay. Both cytotoxic and non-toxic concentrations of t-butylhydroperoxide, hydrogen peroxide and menadione were examined. At non-cytotoxic concentrations, no AO transformation of these cells from interleukin-3 dependence to factor independence (FI) was observed, even after as many as 25 treatments. At cytotoxic concentrations, however, all 3 classes of AO transformed the cells to FI growth. The most potent agent was t-butyl hydroperoxide (43-fold induction), followed by hydrogen peroxide and then menadione. As little as one exposure to cytotoxic levels of these oxidants induced significant transformation, with relative potencies the same as those observed for multiple exposures. These inductions were not due to general cytotoxic effects, since sodium fluoride and heat-shock treatment gave minimal inductions. AO-induced colonies in methylcellulose that were removed, examined and then injected into pre-irradiated mice uniformly produced tumors. Control, non-treated cells did not form tumors. Tumorigenic cells did not form colonies in methylcellulose at lower plating densities. Furthermore, low numbers of transformed cells supplemented to high density with normal cells showed a small but insufficient increase in colony number as compared with high-density cultures of transformed cells. Our results suggest that the transformants depend upon a paracrine mechanism of growth that is mediated by the transformed cells.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Enzyme Applications, Therapeutic

Jayaram¹,

Ahluwalia²,

Cooney³

2000

Kirk-Othmer Encyclopedia of Chemical Technology

View full text Add to dashboard Cite

Enzymes are used for the treatment of a broad variety of diseases by virtue of the fact that they catalyze chemical reactions with great speed and specificity. The principal therapeutic applications of enzymes are as thrombolytic agents capable of rapidly lysing the clots which cause, or contribute to, myocardial infarction, phlebitis, pulmonary embolisms, occluded catheters, and allied conditions; as oral or parenteral replacement therapy for genetic diseases attributable to a deficiency of a specific enzyme or family of enzymes; in oncology, for the control of the growth of select neoplasms or leukemias; and as antidotes to poisons or as counteragents capable of mitigating the delirious effects of toxins, etc. With the advent of DNA technology, strategies for preparing enzymes of human origin for human use have become readily available, thus circumventing the dual problems of immunogenicity and toxicity which are often encountered with enzyme‐proteins of bacterial origin. Making projections to the future, it is anticipated that therapeutic enzymes of human origin will play an increasingly important role in future strategies for controlling a variety of disease states.

show abstract

Protection of bone marrow progenitor cells by superoxide dismutase

Cited by 11 publications

References 15 publications

Nrf2 promotes survival following exposure to ionizing radiation

Nrf2 promotes survival following exposure to ionizing radiation

Active oxygen transforms murine myeloid progenitor cells in vitro

Enzyme Applications, Therapeutic

Contact Info

Product

Resources

About