Human Cu/Zn Superoxide Dismutase ELISA Kit (ab119520)


  • Product nameHuman Cu/Zn Superoxide Dismutase ELISA Kit
  • Detection methodColorimetric
  • Precision
    Sample n Mean SD CV%
    Overall 5.1%
    Sample n Mean SD CV%
    Overall 5.8%
  • Tests
    1 x 96 test
  • Sample type
    Cell culture supernatant, Urine, Serum, Plasma
  • Assay typeSandwich (quantitative)
  • Sensitivity
    0.04 ng/ml
  • Range
    0.08 ng/ml - 5 ng/ml
  • Recovery

    98 %

    Sample specific recovery
    Sample type Average % Range
    Serum 98 89% - 108%

  • Assay durationMultiple steps standard assay
  • Species reactivity
    Reacts with: Human
  • Product overview

    Abcam’s Cu/Zn Superoxide Dismutase Human in vitro ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for accurate quantitative measurement of Human Cu/Zn Superoxide Dismutase concentrations in Cell culture supernatant, serum and plasma (EDTA, citrate, heparin), amniotic fluid, fetal umbilical vein blood and urine.

    Cu/Zn Superoxide Dismutase specific antibodies have been precoated onto 96-well plates. Standards and test samples are added to the wells along with a Cu/Zn Superoxide Dismutase HRP-conjugated detection antibody and the microplate is then incubated at room temperature. After the removal of unbound proteins by washing, TMB is added and catalyzed by HRP to produce a blue color product that changes to yellow after addition of an acidic stop solution. The density of yellow coloration is directly proportional to the Cu/Zn Superoxide Dismutase amount of sample captured in plate.

  • Notes

    ab119520 Cu/Zn Superoxide Dismutase Human ELISA kit has been shown to detect both SOD1 and SOD3.

  • Tested applicationsSuitable for: Sandwich ELISAmore details
  • PlatformMicroplate


  • FunctionDestroys radicals which are normally produced within the cells and which are toxic to biological systems.
  • Involvement in diseaseDefects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1) [MIM:105400]. ALS1 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms.
  • Sequence similaritiesBelongs to the Cu-Zn superoxide dismutase family.
  • Post-translational
    Unlike wild-type protein, the pathogenic variants ALS1 Arg-38, Arg-47, Arg-86 and Ala-94 are polyubiquitinated by RNF19A leading to their proteasomal degradation. The pathogenic variants ALS1 Arg-86 and Ala-94 are ubiquitinated by MARCH5 leading to their proteasomal degradation.
    The ditryptophan cross-link at Trp-33 is reponsible for the non-disulfide-linked homodimerization. Such modification might only occur in extreme conditions and additional experimental evidence is required.
  • Cellular localizationCytoplasm. The pathogenic variants ALS1 Arg-86 and Ala-94 gradually aggregates and accumulates in mitochondria.
  • Information by UniProt
  • Alternative names
    • ALS
    • ALS1
    • Cu/Zn superoxide dismutase
    • homodimer
    • hSod1
    • Indophenoloxidase A
    • IPOA
    • SOD
    • SOD soluble
    • SOD1
    • SOD3
    • Superoxide dismutase [Cu-Zn]
    • Superoxide dismutase 1
    • Superoxide dismutase 1 soluble
    • Superoxide dismutase 3
    • Superoxide dismutase cystolic
    see all
  • Database links


Our Abpromise guarantee covers the use of ab119520 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
Sandwich ELISA Use at an assay dependent concentration.

Human Cu/Zn Superoxide Dismutase ELISA Kit images

  • Representative Standard Curve using ab119520.


References for Human Cu/Zn Superoxide Dismutase ELISA Kit (ab119520)

ab119520 has not yet been referenced specifically in any publications.

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