Mitochondrial changes induced by diphtheria toxin in chicken embryo heart cell cultures

1966 ◽  
Vol 22 (6) ◽  
pp. 373-374 ◽  
Author(s):  
F. Paradisi
Keyword(s):  
Cell Cultures ◽  
Chicken Embryo ◽  
Diphtheria Toxin ◽  
Heart Cell ◽  
Embryo Heart

scholarly journals STUDIES ON THE MODE OF ACTION OF DIPHTHERIA TOXIN

1967 ◽  
Vol 126 (6) ◽  
pp. 1079-1086 ◽  
Author(s):  
Peter F. Bonventre ◽  
John G. Imhoff
Keyword(s):  
Protein Synthesis ◽  
Guinea Pig ◽  
Cell Cultures ◽  
Diphtheria Toxin ◽  
Neonatal Rat ◽  
Heart Cell ◽  
Heart Cells ◽  
Guinea Pig Heart ◽  
Cardiac Tissues ◽  
Toxin Protein

Primary heart cell cultures of embryonic guinea pigs and the neonatal rat were established and incubated with purified diphtheria toxin. The rat heart cell cultures were refractory to the effects of the toxin; protein synthesis proceeded normally as measured by the incorporation of tritiated leucine into cell proteins; beating heart cells continued to contract; and the cell monolayers remained intact after exposure to the toxin for periods as long as 72 hr. These findings are compatible with the species resistance of the rat to diphtheria toxin. The guinea pig heart cell cultures were found to be extremely sensitive to the toxin. Protein synthesis was inhibited by approximately 50% after incubation with small quantities of toxin for 3 hr. Increasing the concentration of the length of exposure to the toxin did not increase this inhibition significantly. In addition, diphtheria toxin exerted a true cytopathic effect on the guinea pig heart cells. Monolayers were destroyed when incubated with the toxin for 2 to 3 days. The results show that the heart cells reflect species resistance or sensitivity to diphtheria toxin in the absence of neural or endocrine influences and suggest further that the toxin exerts a direct toxicity to muscle cells of the heart. It is not yet possible to explain in biochemical terms why the toxin seems to act specifically on cardiac tissues.

scholarly journals Capripoxviruses: Exploring the genetic relatedness between field and vaccine strains from Egypt

2019 ◽  
Vol 12 (12) ◽  
pp. 1924-1930
Author(s):  
Sherin Reda Rouby ◽  
Abdel-Hamid Bazid ◽  
Momtaz Wasfy ◽  
Magdy El-Sayed
Keyword(s):  
Cell Cultures ◽  
Vaccine Strain ◽  
Virus Isolation ◽  
Genetic Relatedness ◽  
Phylogenetic Analyses ◽  
Heart Cell ◽  
Fetal Kidney ◽  
Field Isolates ◽  
Gpcr Gene ◽  
Ovine Fetal

Background and Aim: Lumpy skin disease (LSD) and sheep pox are economically important Capripoxvirus-induced diseases of cattle and sheep, respectively. Despite the extensive vaccination program adopted by Egyptian veterinary authorities, LSD and sheep pox are still prevalent and spread throughout the whole country. The current study was designed for molecular characterization and phylogenetic analysis of LSD virus (LSDV) and Sheep pox virus (SPPV) recovered from field cases in Egypt along with vaccinal strains to assess their genetic relatedness. Materials and Methods: Skin biopsies were collected from naturally infected cases of LSD in Ismailia (n=3 farms) and Beni-Suef (n=2 farms) Governorates and sheep pox in Beni-Suef (n=1 flock). Virus isolation was carried out on primary ovine fetal kidney and heart cell cultures. DNA was extracted from infected materials (skin lesions, infected cell cultures) as well as LSDV Neethling vaccine strain and Romanian SPPV vaccine strain. Polymerase chain reaction was performed using oligonucleotide primers targeting the entire open reading frame of G protein-coupled receptors (GPCR) gene and gene sequences were analyzed. Results: Virus isolation on primary ovine fetal kidney and heart cell culture revealed a cytopathic effect at the third passage characterized by rounding of infected cells and margination of nuclear chromatin. Comparative sequence analysis of GPCR gene revealed that Egyptian LSDV isolated from Ismailia and Beni-Suef shared 99:100% nucleotide and amino acid (AA) identities with each other. In comparison to the vaccinal strains, Egyptian LSDV isolates shared 98:99 nucleotide and AA identities with LSDV Neethling vaccine strain and 93:94% with SPPV Romanian vaccine strain. No differences at the nucleotide or AAs were observed between the SPPV vaccine and virulent strains (100% identity). Phylogenetic analyses revealed that LSDV Neethling vaccine strain is more related to field Egyptian LSDV and clustered within the LSDV group while Romanian SPPV vaccine strain clustered in a separate clade with SPPV field isolates. Conclusion: Comparative sequencing and phylogenetic analyses of the GPCR gene reveal a minimal genetic variation between LSDV field isolates from different locations and a close relationship between virulent field strains and homologous vaccines.

Metabolism of palmitate by anoxic and reoxygenated heart cell cultures

1983 ◽  
Vol 60 (1) ◽  
pp. 209-216
Author(s):  
P.J. Bailey ◽  
T.J. Higgins
Keyword(s):  
Fatty Acid ◽  
Cell Cultures ◽  
Mitochondrial Function ◽  
Cardiac Tissue ◽  
Neutral Lipids ◽  
Heart Cell ◽  
Contributory Factor ◽  
Triglyceride Fraction ◽  
Hypoxic Injury ◽  
Exogenous Lipid

Under anoxic incubation conditions heart cell cultures showed enhanced uptake of [U-14C]palmitic acid into neutral lipids, while incorporation into phospholipids was unaltered. Fractionation of the neutral lipids showed greatest incorporation of radiolabel into the triglyceride fraction. Uptake of fatty acid in normoxic cultures may be dependent upon the supply of glycerol 3-phosphate from glycolysis, as 2-deoxyglucose and L-lactate, respectively, inhibited and stimulated incorporation of fatty acid into neutral lipid fractions. When previously anoxic cultures were reoxygenated, oxidation of fatty acid was depressed and the mitochondrial function of anoxic cultures appeared to be more readily uncoupled by 2,4-dinitrophenol, in comparison with cultures maintained under normoxic conditions. Similar behaviour was seen when oxidation of endogenous lipid or oxidation of glucose was examined. Previously anoxic cultures show a preference for oxidation of endogenous rather than exogenous lipid substrates. The results suggest that anoxia-stimulated lipid accumulation may prove injurious to subsequent mitochondrial function and may be a contributory factor in the pathological processes associated with hypoxic injury of cardiac tissue.

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