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Biology subjects

Madawala, R.

Publications and source records attributed to Madawala, R..

2 recordsLinked to original sources

Chemotherapy accelerated bone ageing is reversed by NMN

Cancer patients face an array of long-term chronic diseases and accelerated biological ageing, due largely to the off-target effects of broadly cytotoxic chemotherapy drugs. This is especially a problem in children, where cancer survivors experience a subsequent high risk of bone mineral deficits and fractures, normally seen in the older population. Here, we model this to show that early-life treatment with a single dose of the commonly used chemotherapy cisplatin profoundly impairs late-life bone health, and that these bone deficits are completely resolved through treatment with the nicotinamide adenine dinucleotide (NAD+) precursor nicotinamide mononucleotide (NMN). While we had previously shown that this same strategy protects against chemotherapy induced female infertility, this maintenance of aged bone health appears to be unrelated to endocrine changes due to protection of the ovarian reserve. Rather, this is driven by altered phosphorus homeostasis and protection against renal damage, which otherwise increases parathyroid hormone secretion to mobilise calcium stores from bone. Overall, this work highlights a new approach for maintaining healthy bone ageing in cancer survivors.

physiology↗

CD38 mediates nicotinamide mononucleotide (NMN) base exchange to yield nicotinic acid mononucleotide (NaMN)

Nicotinamide mononucleotide (NMN) is a widely investigated metabolic precursor to the prominent redox cofactor nicotinamide adenine dinucleotide (NAD+), where it is assumed that delivery of this compound results in its direct incorporation into NAD+ via the canonical salvage / recycling pathway. Surprisingly, treatment with this salvage pathway intermediate leads to increases in nicotinic acid mononucleotide (NaMN) and nicotinic acid adenine dinucleotide (NaAD), two members of the Preiss-Handler / de novo pathways. In mammals, these pathways are not known to intersect prior to the production of NAD+. Here, we show that the cell surface enzyme CD38 can mediate a base exchange reaction on NMN, whereby the nicotinamide ring is exchanged with a free nicotinic acid to yield the Preiss-Handler / de novo pathway intermediate NaMN, with in vivo small molecule inhibition of CD38 abolishing the NMN-induced increase in NaMN and NaAD. Together, these data demonstrate a new mechanism by which the salvage pathway and Preiss-Handler / de novo pathways can exchange intermediates in mammalian NAD+ biosynthesis.

biochemistry↗