Hemoglobin shady grove: A novel fetal methemoglobin variant

Marks, Asher; Luo, Hong-Yuan; Chui, David H.K.; Greenberg, Jay

doi:10.1002/pbc.24503

Cited by 2 publications

(1 citation statement)

References 9 publications

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“…3.6.9.8. Specific susceptible population groups Increased methaemoglobinaemia is reported to occur in patients with a genetic defect of cytochrome b5 reductase types 1 and 2 (Percy and Lappin, 2008;Lorenzo et al, 2011) and in patients with hereditary methaemoglobinaemia, an autosomal dominant disorder caused by mutations in the globin chains, called haemoglobin M (Hb M) disease with at least 10 known mutations, occurring in either the a, b, or g globin genes (Marks et al, 2013). Neonates and infants have a reduced level of cytochrome b5 reductase (about 50-60% of the adult level) (Ross, 1963;Bartos and Desforges, 1966).…”

Section: Assessment Of Mode Of Actionmentioning

confidence: 99%

Re‐evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives

Mortensen¹,

Aguilar²,

Crebelli³

et al. 2017

EFS2

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The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re-evaluating the safety of potassium nitrite (E 249) and sodium nitrite (E 250) when used as food additives. The ADIs established by the SCF (1997) and by JECFA (2002) for nitrite were 0-0.06 and 0-0.07 mg/kg bw per day, respectively. The available information did not indicate in vivo genotoxic potential for sodium and potassium nitrite. Overall, an ADI for nitrite per se could be derived from the available repeated dose toxicity studies in animals, also considering the negative carcinogenicity results. The Panel concluded that an increased methaemoglobin level, observed in human and animals, was a relevant effect for the derivation of the ADI. The Panel, using a BMD approach, derived an ADI of 0.07 mg nitrite ion/kg bw per day. The exposure to nitrite resulting from its use as food additive did not exceed this ADI for the general population, except for a slight exceedance in children at the highest percentile. The Panel assessed the endogenous formation of nitrosamines from nitrites based on the theoretical calculation of the NDMA produced upon ingestion of nitrites at the ADI and estimated a MoE > 10,000. The Panel estimated the MoE to exogenous nitrosamines in meat products to be < 10,000 in all age groups at high level exposure. Based on the results of a systematic review, it was not possible to clearly discern nitrosamines produced from the nitrite added at the authorised levels, from those found in the food matrix without addition of external nitrite. In epidemiological studies there was some evidence to link (i) dietary nitrite and gastric cancers and (ii) the combination of nitrite plus nitrate from processed meat and colorectal cancers. There was evidence to link preformed NDMA and colorectal cancers.

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