PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 21150

Studies on avian erythrocyte metabolism. VII. Effect of inositol pentaphosphate and other organic phosphates on oxygen affinity of the embryonic and adult-type hemoglobins of the turkey embryo.

R E Isaacks·D R Harkness·P H Goldman·J L Adler·C Y Kim
View original source ↗Export metadata ↓

Abstract

The effects of 2, 3-diphosphoglyceric acid (2, 3-DPG), adenosine triphosphate (ATP), inositol tetraphosphate (ITP), inositol pentaphosphate (IPP), and inositol hexaphosphate (IHP) on oxygen affinity of whole stripped hemoglobin (WSH), hemoglobin H (Hb-H; hatching hemoglobin), hemoglobin A (Hb-A), and hemoglobin D (Hb-D) isolated from erythrocytes (RBC) of the 25-day turkey embryo have been studied. The order of the decrease in oxygen affinity induced by these organic phosphates, at molar ratios of phosphate compound to hemoglobin (tetramer) between 2 and 4, is 2, 3-DPG less than ATP less than ITP less than IPP less than IHP. 2, 3-DPG shows a slightly greater effect on reducing oxygen affinity of Hb-H than on either adult-type hemoglobin. The effect of IPP upon lowering the oxygen affinity of either WSH, Hb-H, Hb-A, or Hb-D is approximately 20 percent less than IHP. The effects of the various organic phosphates upon the Hill constant, n, of these purified hemoglobins is variable but appears to reach a maximum when the molar ratio of organic phosphate to hemoglobin (tetramer) is 2 or greater. None of the physiologically occurring organic phosphates has a significant preferential interaction with any specific hemoglobin. These experiments strengthen and support our earlier conclusion, that the changes in whole blood oxygen affinity which occur during avian development result from the changes in composition of the intraerythrocytic organic phosphates.

Explore related subjects

Adenosine DiphosphateAnimalsDiphosphoglyceric AcidsElectrophoresis, Cellulose AcetateEmbryo, NonmammalianErythrocytesFemaleHemoglobinsHydrogen-Ion ConcentrationInositol PhosphatesOxygenPregnancySugar PhosphatesTurkeysJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R E Isaacks, D R Harkness, P H Goldman, J L Adler, C Y Kim. 1977. Studies on avian erythrocyte metabolism. VII. Effect of inositol pentaphosphate and other organic phosphates on oxygen affinity of the embryonic and adult-type hemoglobins of the turkey embryo.. https://doi.org/10.3109/03630267709003422

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2022

A novel DPH5-related diphthamide-deficiency syndrome causing embryonic lethality or profound neurodevelopmental disorder.

PURPOSE: Diphthamide is a post-translationally modified histidine essential for messenger RNA translation and ribosomal protein synthesis. We present evidence for DPH5 as a novel cause of embryonic lethality and profound neurodevelopmental delays (NDDs). METHODS: Molecular testing was performed using exome or genome sequencing. A targeted Dph5 knockin mouse (C57BL/6Ncrl-Dph5em1Mbp/Mmucd) was created for a DPH5 p.His260Arg homozygous variant identified in 1 family. Adenosine diphosphate-ribosylation assays in DPH5-knockout human and yeast cells and in silico modeling were performed for the identified DPH5 potential pathogenic variants. RESULTS: DPH5 variants p.His260Arg (homozygous), p.Asn110Ser and p.Arg207Ter (heterozygous), and p.Asn174LysfsTer10 (homozygous) were identified in 3 unrelated families with distinct overlapping craniofacial features, profound NDDs, multisystem abnormalities, and miscarriages. Dph5 p.His260Arg homozygous knockin was embryonically lethal with only 1 subviable mouse exhibiting impaired growth, craniofacial dysmorphology, and multisystem dysfunction recapitulating the human phenotype. Adenosine diphosphate-ribosylation assays showed absent to decreased function in DPH5-knockout human and yeast cells. In silico modeling of the variants showed altered DPH5 structure and disruption of its interaction with eEF2. CONCLUSION: We provide strong clinical, biochemical, and functional evidence for DPH5 as a novel cause of embryonic lethality or profound NDDs with multisystem involvement and expand diphthamide-deficiency syndromes and ribosomopathies.

Adenosine Diphosphate↗
PubMed1979

Stimulatory and inhibitory effects of dimethylsulfoxide, propranolol and chlorpromazine on the partial reactions of ATPase of sarcoplasmic reticulum.

The effects of dimethylsulfoxide, propranolol and chlorpromazine on the partial reactions of the ATPase of sarcoplasmic reticulum were investigated. When analyzed according to a reaction scheme in which the ADP-sensitive (E1P) and ADP-insensitive (E2P) phosphoenzymes occur sequentially and P1 is derived from the latter, dimethylsulfoxide decreased the rate of E2P hydrolysis whereas it stimulated the rate of the E1P to E2P conversion. Propranolol increased the rate of E2P hydrolysis while it decreased the rate of the E1P to E2P conversion. Propranolol exerted an additional effect, presumably inhibition of the phosphoenzyme formation. These effects of dimethylsulfoxide and propranolol can account for both the stimulatory and inhibitory effects of these drugs on the overall rate of ATP hydrolysis observed in the presence and absence of added alkali metal salts. Chlorpromazine accelerated E2P hydrolysis whereas it appeared to inhibit the E1P to E2P conversion. These effects of chlorpromazine appear able to account for its stimulatory and inhibitory effects on the overall rate of ATP hydrolysis in the presence and absence of alkali metal salts. In the presence of chlorpromazine, however, the rate of Pi liberation during the steady state ATP hydrolysis was found to be greater than the hydrolysis rate of E2P. This finding suggests that under these conditions Pi is derived not only from E2P but also from source(s) other than E2P.

Adenosine Diphosphate↗