Inhibitory effects of niacin and its analogues on induction of ornithine decarboxylase activity by diethylnitrosamine in rat liver

Sakamoto, Mitsuaki; Yanagi, Susumu; Kamiya, Tomoya

doi:10.1016/0006-2952(87)90217-6

Cited by 6 publications

(3 citation statements)

References 23 publications

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“…Protein content in BALF supernatant was determined by the method of Lowry et al (36). 0 2 WEEKS 1601 (7) (20) (8) (20) (18) (22) (20) (20) ss NS SB NB…”

Section: Cell Count and Protein Determination In Lavagementioning

confidence: 99%

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Niacin attenuates bleomycin‐induced lung fibrosis in the hamster

Wang

Giri

Hyde

et al. 1990

J. Biochem. Toxicol.

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Bleomycin (BLM)-induced lung fibrosis has been shown to be accompanied by the activation of poly(ADP-ribose) polymerase and depletion of nicotinamide adenine dinucleotide (NAD) in the lung. Niacin, a precursor of NAD, was used in the present study to investigate its possible ameliorating effect on BLM-induced pulmonary fibrosis in hamsters. Niacin (500 mg/kg IP) or saline (IP) was injected daily for 16 or 23 days. On day 3, hamsters were treated with BLM (7.5 U/5 mL/kg) or an equivalent volume of saline intratracheally. BLM alone significantly increased lung hydroxyproline levels, bronchoalveolar lavage fluid protein concentration, and various inflammatory cell counts in the lavage in both experiments. In addition, BLM alone elevated prolyl hydroxylase and poly(adenosine-5'-diphosphate [ADP]-ribose) polymerase activities in the 3-week study. Niacin treatment significantly decreased BLM-elevated lung hydroxyproline, prolyl hydroxylase, and poly(ADP-ribose) polymerase activities. Histopathology revealed that niacin treatment attenuated BLM-induced thickened alveolar septa, foci of fibrotic consolidation, and accumulations of inflammatory cells in the parenchyma and air spaces. The ability of niacin to attenuate BLM-induced lung fibrosis in hamsters suggests that it may have potential as an antifibrotic agent in humans.

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“…Protein content in BALF supernatant was determined by the method of Lowry et al (36). 0 2 WEEKS 1601 (7) (20) (8) (20) (18) (22) (20) (20) ss NS SB NB…”

Section: Cell Count and Protein Determination In Lavagementioning

confidence: 99%

“…Attempts to study the effects of NAD in vivo were unsuccessful due to the toxicity, instability, and inability of this compound to gain intracellular access (20). However, niacin (nicotinic acid), an established precursor of the nicotinamide nucleotide coenzymes, NAD and NAD phosphate (NADP) (21) might be an ideal alternative.…”

Section: Introductionmentioning

confidence: 99%

Niacin attenuates bleomycin‐induced lung fibrosis in the hamster

Wang

Giri

Hyde

et al. 1990

J. Biochem. Toxicol.

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“…The safety of nicotinaldehyde could be most probably explained by the existence, in mice as well as in humans, of a large number of aldehyde metabolizing enzymes, as mentioned above. In line with this assumption, several reported studies in which rats were fed diets supplemented with nicotinaldehyde have been carried out without toxicity while showing significant activities comparable to NA at the same doses [26,30].…”

Section: Discussionmentioning

confidence: 72%

Nicotinaldehyde, a Novel Precursor of NAD Biosynthesis, Abrogates the Anti-Cancer Activity of an NAD-Lowering Agent in Leukemia

Matsumoto

Biniecka

Bellotti

et al. 2023

Cancers

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Targeting NAD depletion in cancer cells has emerged as an attractive therapeutic strategy for cancer treatment, based on the higher reliance of malignant vs. healthy cells on NAD to sustain their aberrant proliferation and altered metabolism. NAD depletion is exquisitely observed when NAMPT, a key enzyme for the biosynthesis of NAD, is inhibited. Growing evidence suggests that alternative NAD sources present in a tumor environment can bypass NAMPT and render its inhibition ineffective. Here, we report the identification of nicotinaldehyde as a novel precursor that can be used for NAD biosynthesis by human leukemia cells. Nicotinaldehyde supplementation replenishes the intracellular NAD level in leukemia cells treated with NAMPT inhibitor APO866 and prevents APO866-induced oxidative stress, mitochondrial dysfunction and ATP depletion. We show here that NAD biosynthesis from nicotinaldehyde depends on NAPRT and occurs via the Preiss–Handler pathway. The availability of nicotinaldehyde in a tumor environment fully blunts the antitumor activity of APO866 in vitro and in vivo. This is the first study to report the role of nicotinaldehyde in the NAD-targeted anti-cancer treatment, highlighting the importance of the tumor metabolic environment in modulating the efficacy of NAD-lowering cancer therapy.

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Prevention of Cancer by Vitamin B3 (Nicotinamide and Nicotinic Acid)

Troll

1993

Protease Inhibitors as Cancer Chemopreventive Agents

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Inhibitory effects of niacin and its analogues on induction of ornithine decarboxylase activity by diethylnitrosamine in rat liver

Cited by 6 publications

References 23 publications

Niacin attenuates bleomycin‐induced lung fibrosis in the hamster

Niacin attenuates bleomycin‐induced lung fibrosis in the hamster

Nicotinaldehyde, a Novel Precursor of NAD Biosynthesis, Abrogates the Anti-Cancer Activity of an NAD-Lowering Agent in Leukemia

Prevention of Cancer by Vitamin B3 (Nicotinamide and Nicotinic Acid)

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