Related Experiment Video

Updated: Jun 20, 2026

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

Manganese corroles prevent intracellular nitration and subsequent death of insulin-producing cells

Zoya Okun1, Lana Kupershmidt, Tamar Amit

  • 1Schulich Faculty of Chemistry, Technion-Israel Institute of Technology, Haifa 32000, Israel.

ACS Chemical Biology
|September 1, 2009
PubMed

Insights

Manganese(III) corroles offer unprecedented protection for pancreatic beta cells against nitration and cell death, a key factor in diabetes mellitus. This novel strategy surpasses traditional antioxidants by preventing damaging protein nitration.

Area of Science:

  • Biochemistry
  • Medicinal Chemistry
  • Endocrinology

Background:

  • Reactive oxygen species contribute significantly to diabetes mellitus (DM) pathogenesis.
  • Insulin-producing beta cells are highly susceptible to free-radical damage.
  • Preventing protein nitration is a promising therapeutic strategy for DM.

Purpose of the Study:

  • To evaluate the efficacy of manganese(III) corroles in protecting pancreatic beta cells.
  • To investigate their role in preventing intracellular nitration and cell death.
  • To compare their performance against analogous porphyrin metal complexes.

Main Methods:

  • Treatment of rat pancreatic beta cells with peroxynitrite.
  • Assessment of cell viability and intracellular nitration levels.
  • Comparative analysis of manganese(III) corroles and porphyrin metal complexes.

Main Results:

  • Manganese(III) corroles demonstrated unprecedented efficiency in protecting beta cells.
  • A positively-charged manganese(III) corrole rapidly decomposed peroxynitrite via a unique mechanism.
  • This mechanism avoided potentially nitrating reaction intermediates, unlike porphyrins.

Conclusions:

  • Manganese(III) corroles represent a superior strategy for protecting beta cells from nitrative stress.
  • Their unique catalytic mechanism offers significant advantages over traditional antioxidants.
  • This finding opens new avenues for therapeutic interventions in diabetes mellitus.

More Related Videos

In vivo Imaging of Optic Nerve Fiber Integrity by Contrast-Enhanced MRI in Mice11:38

In vivo Imaging of Optic Nerve Fiber Integrity by Contrast-Enhanced MRI in Mice

Published on: July 22, 2014

Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...