Bone manganese is a sensitive biomarker of ongoing elevated manganese exposure, but does not accumulate across the lifespan.

Studies have established associations between environmental and occupational manganese (Mn) exposure and executive and motor function deficits in children, adolescents, and adults. These health risks from elevated Mn exposure underscore the need for effective exposure biomarkers to improve exposure classification and help detect/diagnose Mn-related impairments. Here, neonate rats were orally exposed to 0, 25, or 50 mg Mn/kg/day during early life (PND 1-21) or lifelong through âˆ¼ PND 500 to determine the relationship between oral Mn exposure and blood, brain, and bone Mn levels over the lifespan, whether Mn accumulates in bone, and whether elevated bone Mn altered the local atomic and mineral structure of bone, or its biomechanical properties. Additionally, we assessed levels of bone Mn compared to bone lead (Pb) in aged humans (age 41-91) living in regions impacted by historic industrial ferromanganese activity. The animal studies show that blood, brain, and bone Mn levels naturally decrease across the lifespan without elevated Mn exposure. With elevated exposure, bone Mn levels were strongly associated with blood Mn levels, bone Mn was more sensitive to elevated exposures than blood or brain Mn, and Mn did not accumulate with lifelong elevated exposure. Elevated early life Mn exposure caused some changes in bone mineral properties, including altered local atomic structure of hydroxyapatite, along with some biomechanical changes in bone stiffness in weanlings or young adult animals. In aged humans, blood Mn ranged from 5.4 to 23.5 ng/mL; bone Mn was universally low, and decreased with age, but did not vary based on sex or female parity history. Unlike Pb, bone Mn showed no evidence of accumulation over the lifespan, and may not be a biomarker of cumulative long-term exposure. Thus, bone may be a useful biomarker of recent ongoing Mn exposure in humans, and may be a relatively minor target of elevated exposure.

Tooth manganese as a biomarker of exposure and body burden in rats.

BACKGROUND: Neonates and children are particularly vulnerable to the toxic effects of excess manganese (Mn), but studies of Mn exposure during these developmental periods are hampered by a lack of validated biomarkers. Deciduous teeth may be used to assess Mn exposure during these developmental periods but require further validation to determine the relationship between tooth Mn, Mn in target tissues, and exposure. OBJECTIVES: To determine the relationship of tooth Mn concentrations with: (i) exposure dose, (ii) the timing/duration of exposure, and (iii) with Mn concentrations in blood, brain and bone. METHODS: Rats in different treatment groups were orally exposed to 0, 25 or 50µg/g/day Mn either from postnatal day (PND) 1 - 21 and culled at PND 24, from PND 1 - 21 and culled as adults (>PND 290), or from PND 1 - throughout life and culled at >290 PND. Mn was measured in second molars, femurs, brain and blood by ICP-MS. RESULTS: Tooth Mn increased significantly with dose in rats exposed for 21 PND and culled at 24 PND (p<0.001). In rats culled at >290 PND, tooth Mn increased with exposure duration (p<0.001) and reflected exposure duration. A significant, positive association between tooth Mn and Mn levels in blood (Spearman's rho 0.69, p<0.01) brain (rho 0.59, p<0.05) and bone (rho 0.69, p<0.01) was observed in animals with lifelong exposure. Tooth Mn and Mn levels in bone were also significantly positively associated in animals exposed only early in life (rho 0.76, p<0.001). CONCLUSIONS: Teeth are a sensitive biomarker of active and past Mn exposure and Mn burden in tissues. Unlike blood, teeth retain information on exposure history over the short and long-term.

An electron transfer driven magnetic switch: ferromagnetic exchange and spin delocalization in iron verdazyl complexes.

The verdazyl 'pincer' ligand, 1-isopropyl-3,5-dipyridyl-6-oxoverdazyl (dipyvd), coordinates iron to form a series of pseudooctahedral coordination compounds [Fe(dipyvd)2]n+ (n = 0-3). In the case where n = 2, the molecular geometry and physical and spectral properties are consistent with a low spin (S = 0) iron(ii) ion coordinated by two ferromagnetically coupled radical ligands. Upon one electron reduction, the room temperature effective magnetic moment of the complex jumps from µeff = 2.64 to µeff = 5.86 as a result of spin crossover of the iron atom combined with very strong ferromagnetic coupling of the remaining ligand centered unpaired electron with the metal center. The sign of the exchange is opposite to that observed in other high spin iron/radical ligand systems and appears to be a result of delocalization of the ligand unpaired electron across the whole molecule. The large change in magnetic properties, combined with a delocalized electronic structure and accessible redox potentials, suggests the utility of this and related systems in the development of novel molecular spintronic devices.

Correction: An electron transfer driven magnetic switch: ferromagnetic exchange and spin delocalization in iron verdazyl complexes.

Correction for 'An electron transfer driven magnetic switch: ferromagnetic exchange and spin delocalization in iron verdazyl complexes' by David J. R. Brook et al., Dalton Trans., 2018, 47, 6351-6360.

Strong ferromagnetic metal-ligand exchange in a nickel bis(3,5-dipyridylverdazyl) complex.

A new 1,5-dipyridyl verdazyl, synthesized from the corresponding dipyridyl hydrazone, coordinates nickel(ii) to form a structurally characterized, pseudooctahedral complex analogous to Ni(terpy)(2)(2+). The unusually short Ni-verdazyl distance results in strong ferromagnetic exchange (J(Ni-rad) = +300, J(rad-rad) = +160 cm(-1)) between all three paramagnetic species along with a metal-ligand charge transfer band in the electronic spectrum.