Treatment of Wistar rats with a renal carcinogen, ferric nitrilotriacetate, causes DNA-protein cross-linking between thymine and tyrosine in their renal chromatin.
about
Oxidative Decay of DNAExpression of stress-response and cell proliferation genes in renal cell carcinoma induced by oxidative stressTwo distinct mechanisms for loss of thioredoxin-binding protein-2 in oxidative stress-induced renal carcinogenesisReactive oxygen species-induced molecular damage and its application in pathology.Incision of DNA-protein crosslinks by UvrABC nuclease suggests a potential repair pathway involving nucleotide excision repair.Mechanisms of free radical-induced damage to DNA.Iron and thiols as two major players in carcinogenesis: friends or foes?RNA oxidation catalyzed by cytochrome c leads to its depurination and cross-linking, which may facilitate cytochrome c release from mitochondria.Iron as a target of chemoprevention for longevity in humans.Genome-wide assessment of oxidatively generated DNA damage.Iron overload as a major targetable pathogenesis of asbestos-induced mesothelial carcinogenesis.Measurement of oxidatively induced DNA damage and its repair, by mass spectrometric techniques.Mechanisms of chemically induced renal carcinogenesis in the laboratory rodent.Effect of habitual exercise on renal carcinogenesis by ferric nitrilotriacetateAntioxidant biofactor, a processed grain food, inhibits iron nitrilotriacetate-induced renal tumorigenesis, hyperproliferative response, and oxidative damage.An electron spin resonance study on alkylperoxyl radical in thin-sliced renal tissues from ferric nitrilotriacetate-treated rats: the effect of alpha-tocopherol feeding.Vitamin E inhibits hepatic oxidative stress, toxicity and hyperproliferation in rats treated with the renal carcinogen ferric nitrilotriacetate.Habitual exercise induced resistance to oxidative stress.Association of microRNA-34a overexpression with proliferation is cell type-dependent.Nordihydroguairetic acid is a potent inhibitor of ferric-nitrilotriacetate-mediated hepatic and renal toxicity, and renal tumour promotion, in mice.Development of high-grade renal cell carcinomas in rats independently of somatic mutations in the Tsc2 and VHL tumor suppressor genes.Low incidence of point mutations in H-, K- and N-ras oncogenes and p53 tumor suppressor gene in renal cell carcinoma and peritoneal mesothelioma of Wistar rats induced by ferric nitrilotriacetate.
P2860
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P2860
Treatment of Wistar rats with a renal carcinogen, ferric nitrilotriacetate, causes DNA-protein cross-linking between thymine and tyrosine in their renal chromatin.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年学术文章
@wuu
1995年学术文章
@zh-cn
1995年学术文章
@zh-hans
1995年学术文章
@zh-my
1995年学术文章
@zh-sg
1995年學術文章
@yue
1995年學術文章
@zh
1995年學術文章
@zh-hant
name
Treatment of Wistar rats with ...... sine in their renal chromatin.
@en
Treatment of Wistar rats with ...... sine in their renal chromatin.
@nl
type
label
Treatment of Wistar rats with ...... sine in their renal chromatin.
@en
Treatment of Wistar rats with ...... sine in their renal chromatin.
@nl
prefLabel
Treatment of Wistar rats with ...... sine in their renal chromatin.
@en
Treatment of Wistar rats with ...... sine in their renal chromatin.
@nl
P2093
P356
P1476
Treatment of Wistar rats with ...... sine in their renal chromatin.
@en
P2093
P2860
P304
P356
10.1002/IJC.2910620313
P577
1995-07-01T00:00:00Z