Limits...
Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus

Vanadium compounds in the cell. Vanadyl and vanadate enters the cell by passive diffusion and through the anionic channels, respectively. Then, in the cytoplasm vanadyl cations may be subject to Fenton reaction in which vanadate is produced. Vanadate is reduced by intracellular antioxidants to vanadyl cations. Vanadate present in a cell does not occur in the cytoplasm, where it is bound to proteins with free cysteine residues. In the reaction with H2O2 the complexed vanadate irreversibly oxidizes cysteine residues.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4490466&req=5

ijms-16-12648-f002: Vanadium compounds in the cell. Vanadyl and vanadate enters the cell by passive diffusion and through the anionic channels, respectively. Then, in the cytoplasm vanadyl cations may be subject to Fenton reaction in which vanadate is produced. Vanadate is reduced by intracellular antioxidants to vanadyl cations. Vanadate present in a cell does not occur in the cytoplasm, where it is bound to proteins with free cysteine residues. In the reaction with H2O2 the complexed vanadate irreversibly oxidizes cysteine residues.

Mentions: In biological systems vanadium is present in +4 or +5 oxidation states and in ascidians in +3 oxidation state. Under physiological conditions, vanadium in the +4 oxidation state is present in the form of vanadyl cations (VO2+). In the +5 oxidation state it can be found as vanadate ions, e.g., orthovanadate (H2VO4−) [30]. In the bloodstream, vanadium in the +5 oxidation state enters cells through anionic channels while vanadium in the +4 oxidation state reaches cells by passive diffusion and transferrin binding vanadyl cations by endocytosis (Figure 2) [31]. In the cytoplasm, due to the reduction by the intracellular antioxidants, vanadium is present in the +4 oxidation state as vanadyl ions [32,33]. This reaction results in the formation of reactive oxygen species (ROS) which at high vanadate concentrations cause oxidative stress [33,34,35]. In the cytoplasm vanadyl cations are subsequently subject to the Fenton reaction with H2O2 to form vanadate ions and hydroxyl radical HO· [36,37]. Vanadate from this reaction enters the cell and does not appear in the cytoplasm, but instead is bound to proteins at cysteine residues [38]. In this form, vanadate and H2O2 can form pervanadate which directly oxidize thus bound cysteine residues [38,39]. This process is significant in the case of simultaneous exposure to vanadium compounds and substances that cause oxidative stress [40].


Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

Vanadium compounds in the cell. Vanadyl and vanadate enters the cell by passive diffusion and through the anionic channels, respectively. Then, in the cytoplasm vanadyl cations may be subject to Fenton reaction in which vanadate is produced. Vanadate is reduced by intracellular antioxidants to vanadyl cations. Vanadate present in a cell does not occur in the cytoplasm, where it is bound to proteins with free cysteine residues. In the reaction with H2O2 the complexed vanadate irreversibly oxidizes cysteine residues.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490466&req=5

ijms-16-12648-f002: Vanadium compounds in the cell. Vanadyl and vanadate enters the cell by passive diffusion and through the anionic channels, respectively. Then, in the cytoplasm vanadyl cations may be subject to Fenton reaction in which vanadate is produced. Vanadate is reduced by intracellular antioxidants to vanadyl cations. Vanadate present in a cell does not occur in the cytoplasm, where it is bound to proteins with free cysteine residues. In the reaction with H2O2 the complexed vanadate irreversibly oxidizes cysteine residues.
Mentions: In biological systems vanadium is present in +4 or +5 oxidation states and in ascidians in +3 oxidation state. Under physiological conditions, vanadium in the +4 oxidation state is present in the form of vanadyl cations (VO2+). In the +5 oxidation state it can be found as vanadate ions, e.g., orthovanadate (H2VO4−) [30]. In the bloodstream, vanadium in the +5 oxidation state enters cells through anionic channels while vanadium in the +4 oxidation state reaches cells by passive diffusion and transferrin binding vanadyl cations by endocytosis (Figure 2) [31]. In the cytoplasm, due to the reduction by the intracellular antioxidants, vanadium is present in the +4 oxidation state as vanadyl ions [32,33]. This reaction results in the formation of reactive oxygen species (ROS) which at high vanadate concentrations cause oxidative stress [33,34,35]. In the cytoplasm vanadyl cations are subsequently subject to the Fenton reaction with H2O2 to form vanadate ions and hydroxyl radical HO· [36,37]. Vanadate from this reaction enters the cell and does not appear in the cytoplasm, but instead is bound to proteins at cysteine residues [38]. In this form, vanadate and H2O2 can form pervanadate which directly oxidize thus bound cysteine residues [38,39]. This process is significant in the case of simultaneous exposure to vanadium compounds and substances that cause oxidative stress [40].

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus