Modification of Renal Tumorigenic Effect of Streptozotocin by Nicotinamide: Spontaneous Reversibility of Streptozotocin Diabetes

Rakieten, Nathan; Gordon, Benjamin S.; Beaty, Annabel; Cooney, David A.; Schein, Philip S.

doi:10.3181/00379727-151-39209

Cited by 33 publications

(15 citation statements)

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“…Consequently, there were no data available in the literature on urinary levels of high dose nicotinamide over longer periods of time. Nonetheless, high dose nicotinamide has therapeutic value to treat lipid profiles (Handfield-Jones et al, 1988;Takahashi et al, 2004;Zak et al, 2006), diabetes (Rakieten et al, 1976;Wilson and Buchingham, 2001;Yamada et al, 1982;depression (Chouinard et al, 1979), HIV (Murray et al, 2001), renal tumors (Beales et al, 1999), graft failure (Brandhorst et al, 2002), migraines (Gedye, 2001) and as an antioxidant (Kamat and Devasagayam, 1999;Ungerstedt et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Antioxidant metabolism induced by quinic acid. increased urinary excretion of tryptophan and nicotinamide

Pero

Lund

Leanderson

2008

Phytotherapy Research

127

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For over 50 years, hippuric/quinic acids were believed to have no biological efficacy. Here data are presented to support the hypothesis that quinic acid is not responsible for any efficacy, but rather that quinic acid nutritionally supports the synthesis of tryptophan and nicotinamide in the gastrointestinal (GI) tract, and that this in turn leads to DNA repair enhancement and NF-kB inhibition via increased nicotinamide and tryptophan production.Moreover, it is shown that quinic acid is a normal constituent of our diet, capable of conversion to tryptophan and nicotinamide via the GI tract microflora, thus providing an in situ physiological source of these essential metabolic ingredients to humans. The concentrations of quinic and hippuric acids in the diet were dependent on each other when analysed in urine, as was evidenced by a significant linear regression analysis that included unsupplemented control subjects (n = 45, p < 0.001). Thus, these ingredients were identified as major dietary components, and not simply originating from environmental pollution as previously had been thought.

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Section: Discussionmentioning

confidence: 99%

Antioxidant metabolism induced by quinic acid. increased urinary excretion of tryptophan and nicotinamide

Pero

Lund

Leanderson

2008

Phytotherapy Research

127

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“…Intraperitoneal nicotinamide (350 mg/kg) increased the incidence of streptozotocin-induced pancreatic islet-cell tumours in male Holtzman rats from 4% in controls (streptozotocin only) to 64% [48], but it decreased the incidence of renal adenomas from 77% to 18% [49]. Nicotinamide administered intraperitoneally at 500 mg/kg to white male weanling rats before and after administration of pyrrollizidine alkaloid heliotrine increased pancreatic islet-cell tumours [50].…”

Section: Nicotinamide Supplementation and Animal Models Of Carcinomentioning

confidence: 99%

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Surjana

Halliday

Damian

2010

Journal of Nucleic Acids

169

174

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Nicotinamide is a water-soluble amide form of niacin (nicotinic acid or vitamin B3). Both niacin and nicotinamide are widely available in plant and animal foods, and niacin can also be endogenously synthesized in the liver from dietary tryptophan. Nicotinamide is also commercially available in vitamin supplements and in a range of cosmetic, hair, and skin preparations. Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD+), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1). Numerous in vitro and in vivo studies have clearly shown that PARP-1 and NAD+ status influence cellular responses to genotoxicity which can lead to mutagenesis and cancer formation. This paper will examine the role of nicotinamide in the protection from carcinogenesis, DNA repair, and maintenance of genomic stability.

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“…It is well known that SZ induces insulinoma [4,6,9,15,20] and renal tumor [1,16,17] in a high incidence in rats 8-9 months or more after single injection. However, there have been few reports on the induction of other tumors by SZ administration in laboratory animals.…”

Section: Streptozotocinmentioning

confidence: 99%

Neoplastic Lesions in Streptozotocin-treated Rats

Okawa

Doi

1983

Experimental Animals

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Pathological examination was carried out on 16 male Sprague-Dawley rats received single i. v. injection of 60 mg/kg of streptozotocin (SZ) at 5 weeks of age and maintained for 22 months. Insulinoma (63 %), renal adenoma (50 %), hepatocellular tumor (69 %), cholangioma (31 %) and Leydig cell tumor (56 %) were found in a high incidence, and therefore occurrence of these tumors was considered to be attributable to the treatment with SZ. In addition to these tumors, though in a low incidence, various such tumors as leukemia, reticulum cell sarcoma, mammary tumor and glioma were also found.

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Modification of Renal Tumorigenic Effect of Streptozotocin by Nicotinamide: Spontaneous Reversibility of Streptozotocin Diabetes

Cited by 33 publications

References 0 publications

Antioxidant metabolism induced by quinic acid. increased urinary excretion of tryptophan and nicotinamide

Antioxidant metabolism induced by quinic acid. increased urinary excretion of tryptophan and nicotinamide

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Neoplastic Lesions in Streptozotocin-treated Rats

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