Polycythemia Induced in Rats by Intrarenal Injection of Nickel Sulfide Ni3S2

Jasmin, G.; Solymoss, B.

doi:10.3181/00379727-148-38628

Cited by 23 publications

(7 citation statements)

References 2 publications

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“…Erythropoietin synthesis is induced by the transcription factor hypoxiainducible factor 1 (HIF-1). Besides induction by hypoxia, HIF-1 has been induced in vivo and in vitro by the transition metals cobalt, nickel, and manganese (Chandel et al 2000;Jasmin and Solymoss 1975;Goldberg et al 1988). We therefore suggest that the observed increase in RBC concentrations is caused by an HIF-1 induction of erythropoietin, caused by transition metals on the surface of particulate matter.…”

Section: Discussionmentioning

confidence: 82%

Personal PM2.5 Exposure and Markers of Oxidative Stress in Blood

Sørensen¹,

Daneshvar²,

Hansen³

et al. 2002

Environ Health Perspect

208

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Section: Discussionmentioning

confidence: 82%

Personal PM2.5 Exposure and Markers of Oxidative Stress in Blood

Sørensen¹,

Daneshvar²,

Hansen³

et al. 2002

Environ Health Perspect

208

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“…[47][48][49] In original studies in rats, intrarenal injection of nickel resulted in pronounced erythrocytosis. 50,51 The high erythrocyte counts were accompanied by increased EPO production. In vitro exposure of human hepatoma cells (Hep3B or HepG2) to low oxygen, or to increasing amounts of CoCl 2 or NiCl 2 resulted in a dose-dependent enhancement of EPO mRNA expression.…”

Section: Nickel Cobalt and Hypoxic Stressmentioning

confidence: 99%

HIF-1, An Oxygen and Metal Responsive Transcription Factor

Maxwell

Salnikow²

2004

Cancer Biology & Therapy

225

195

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Normal development and function of metazoan organisms depend on oxygen availability. The level of oxygen can be sensed by individual cells, which respond to reduced oxygenation (hypoxia) largely through activation of hypoxia-inducible factor-1 (HIF-1). At the organism level the response to hypoxia involves an increase in red blood cell production. Within tissues, HIF activation increases the blood supply and blood vessel growth. At the individual cell level it is manifested as an increase in anaerobic metabolism in order to sustain basic cellular functions. Iron is central to the oxygen sensing mechanism, and sensitivity to other metals, namely cobalt and nickel, is a distinctive feature of the HIF system; in fact, this is often used as an initial way of implicating HIF-1 in a biological response. Historically, the fact that nickel or cobalt mimicked hypoxia provided an important clue as to the nature of the oxygen sensing mechanism. It also raises the possibility that nickel or cobalt exposure may have important toxic and pathological effects mediated by HIF activation. Here we review the implications of the metal sensitivity of the HIF-1 system, and examine the hypothesis that HIF-1 activation may play an important role in metal induced carcinogenesis.

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“…Histologically, most of the rat renal tumors resembled the sarcomatous variant of the classic renal mesenchymal tumor, while some were composed of poorly differentiated cells [114,273]. Interestingly, the early stage of renal carcinogenesis by Ni 3 S 2 was accompanied by a strong increase in hemoglobin and erythrocyte levels [114,274]. The erythrocytosis was due to the induction of erythropoietin [111,275], a part of the hypoxia-mimicking response to nickel, reviewed in more detail in Chapter 16.…”

Section: Intrarenal Injectionmentioning

confidence: 99%