Microbe-derived antioxidants attenuate cobalt chloride-induced mitochondrial function, autophagy and BNIP3-dependent mitophagy pathways in BRL3A cells

Environmental excessive cobalt (Co) exposure increases risks of public health. This study aimed to evaluate the potential mechanism of microbe-derived antioxidants (MA) blend fermented by probiotics in attenuating cobalt chloride (CoCl2)-induced toxicology in buffalo rat liver (BRL3A) cells. Herein, results showed that some phenolic acids increased in MA compared with the samples before fermentation through UHPLC-QTOF-MS analysis. Also, the contents of essential and non-essential amino acids, their derivatives and minerals were rich in MA. The DPPH, O2, OH and ABTS+ scavenging ability of MA is comparable to those of vitamin C and better than mitoquinone mesylate (mitoQ).
In vitro cell experiments showed that CoCl2 treatment increased the percentage of apoptosis cells, lactate dehydrogenase and genes involved in glycolysis, increased ATP production and decreased mitochondrial membrane potential, increased genes involved in canonical autophagy process (including initiation, autophagosomes maturation and fusion with lysosome) and BNIP3-dependent mitophagy pathways in BRL3A cells, while MA attenuated CoCl2-induced reactive oxygen species (ROS) production, apoptosis, mitochondrial protein expression and dysfunction, and BNIP3-dependent mitophagy. Collectively, these results provide insights into the role of MA in reversing CoCl2-induced toxicology in BRL3A cells, providing the promising constituents for decreasing Co-induced toxicology in functional foods.

Cardioprotective effects of alantolactone on isoproterenol-induced cardiac injury and cobalt chloride-induced cardiomyocyte injury

Objectives: Alantolactone (AL) is a compound extracted from the roots of Inula Racemosa that has shown beneficial effects in cardiovascular disease. However, the cardioprotective mechanism of AL against hypoxic/ischemic (H/I) injury is still unclear. This research aimed to determine AL’s ability to protect the heart against isoproterenol (ISO)-induced MI injury in vivo and cobalt chloride (CoCl2) induced H/I injury in vitro.
Methods: Electrocardiography (ECG), lactate dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI) assays in addition to histological analysis of the myocardium were used to investigate the effects of AL in vivo. Influences of AL on L-type Ca2+ current (ICa-L) in isolated rat myocytes were observed by the patch-clamp technique. Furthermore, cell viability, apoptosis, oxidative stress injury, mitochondrial membrane potential, and intracellular Ca2+ concentration were examined in vitro.
Results: The results indicated that AL treatment ameliorated the morphological and ECG changes associated with MI, and decreased levels of LDH, CK, and cTnI. Furthermore, pretreatment with AL elevated antioxidant enzyme activity and suppressed ROS production. AL prevented H/I-induced apoptosis, mitochondria damage, and calcium overload while reducing ICa-L in a concentration and time dependent fashion. The 50% inhibiting concentration (IC50) and maximal inhibitory effect (Emax) of AL were 17.29 μmol/L and 57.73 ± 1.05%, respectively.
Conclusion: AL attenuated MI-related injury by reducing oxidative stress, apoptosis, calcium overload, and mitochondria damage. These cardioprotective effects may be related to the direct inhibition of ICa-L.
Keywords: L-type calcium channel currents; alantolactone; calcium influx; cardio-protection; oxidative stress.

Tongxin formula protects H9c2 cardiomyocytes from cobalt chloride-induced hypoxic injury via inhibition of apoptosis

In this study, the effect of the Tongxin formula (TXF) on the apoptosis of H9c2 cardiomyocytes induced by cobalt chloride (CoCl2) was investigated, and the potential mechanism was explored. A hypoxic injury model of H9c2 cardiomyocytes was established using CoCl2. The cell viability was measured using a Cell Counting Kit-8 assay. The lactate dehydrogenase (LDH) release and caspase-3 activity were measured using spectrophotometry. The apoptosis was measured via Annexin V-FITC/PI staining and flow cytometry. The changes in the mitochondrial membrane potential were examined using immunofluorescence microscopy following the loading of JC-1 probes.
The expressions of apoptosis-related proteins and key proteins in the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway were examined via immunoblotting. The different TXF concentrations studied significantly improved the percentage of viability of cardiomyocytes with hypoxic injury, and the LDH release, apoptotic rate, caspase-3 activity, and levels of cleaved caspase-3 protein were reduced in the injured cells. Additionally, the TXF group had increased mitochondrial membrane potential, upregulated expression of Bcl-2 and p-Akt proteins, and significantly reduced expression of cleaved caspase-3 protein in the cells with hypoxic injury.
Moreover, in the TXF group, the treatment significantly reduced the BAX protein expression, but the difference was not statistically significant compared with the CoCl2 group. In this study, TXF regulated the expression of apoptosis-related proteins, inhibited apoptosis, increased the mitochondrial membrane potential, and alleviated damage to the mitochondrial membrane, thereby protecting the cardiomyocytes from hypoxic injury. The underlying mechanism could be related to activation of the PI3K/Akt signaling pathway and upregulation of the Bcl-2 protein.

The biological effect of cobalt chloride mimetic-hypoxia on nucleus pulposus cells and the comparability with physical hypoxia in vitro

Objective: Nucleus pulposus cells (NPCs) are cells e induce mimetic-hypoxia for NPCs and the comparison withxtracted from the intervertebral disc and are important for research into intervertebral disc degeneration (IVDD). NPCs live in an avascular and relatively hypoxic environment. Cobalt chloride (CoCl2) has been used in many cell studies to mimic hypoxia. The objective of this study was to explore the possibility of using CoCl2 to hypoxia (1% O2in vitro.
 Materials and methods: Rat nucleus pulposus cells of Passage 3-5 were used in this research. Cell viability, rate of cell apoptosis, ROS (reactive oxygen species) generation, cell migration, extracellular pH and extracellular matrix metabolism were determined to compare the influence of hypoxia (1% O2) and CoCl2 on NPCs.
Results: We found that the effects of CoCl2 on NPCs was dose-dependent. At the proper concentration, CoCl2 could be used to elicit chemical hypoxia for nucleus pulposus cells in vitro and many biological effects, analogous to physical hypoxia (1% O2), could be achieved such as enhanced cell viability, decreased apoptosis and activated extracellular matrix metabolism. On the other hand, CoCl2 mimetic-hypoxia did not affect NPCs glycolysis and migration compared to physical hypoxia. In addition, high concentration of CoCl2 (>200 μM) is harmful to NPCs with high rates of apoptosis and ECM (extracellular matrix) degradation.
 Conclusions: It is feasible and convenient to use CoCl2 to induce chemical mimetic hypoxia for culturing NPCs on the premise of appropriate concentration. But in aspects of cell migration and glycolysis, CoCl2 could not achieve similar results with physical hypoxia. This study may provide a convenient method and enlightenment to induce mimetic-hypoxia for researchers studying NPCs and IVVD.
Keywords: Apoptosis; Cobalt chloride; Extracellular matrix synthesis; Hypoxia; Migration; Nucleus pulposus cells.

Synthesis and structure determination of racemic (Δ/Λ)-tris-(ethyl-enedi-amine)-cobalt(III) trichloride hemi(hexa-aqua-sodium chloride)

The synthesis and crystal structure of the title racemic compound, [Co(C2H8N2)3]Cl3.{[Na(H2O)6]Cl}0.5, are reported. The trivalent cobalt atom, which resides on a crystallographic threefold axis, is chelated by a single ethyl-ene di-amine (en) ligand and yields the tris-chelate [Co(en)3]3+ cation with distorted octa-hedral geometry after the application of crystal symmetry.

Cobalt(II) chloride hexahydrate

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GK0520-100G | 100 g: 51.00 EUR

Cobalt(II) chloride hexahydrate

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GK0520-1KG | 1 kg: 132.00 EUR

Cobalt(II) chloride hexahydrate

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GK0520-250G | 250 g: 66.00 EUR

Cobalt(II) chloride hexahydrate

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GK0520-25G | 25 g: 42.00 EUR

Cobalt(II) chloride hexahydrate

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GK0520-500G | 500 g: 90.00 EUR

Cobalt(II) chloride, anhydrous

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GK0658-100G | 100 g: 74.00 EUR

Cobalt(II) chloride, anhydrous

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GK0658-250G | 250 g: 110.00 EUR

Cobalt(II) chloride, anhydrous

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GK0658-25G | 25 g: 48.00 EUR

Cobalt(II) chloride, anhydrous

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GK0658-500G | 500 g: 174.00 EUR

Cobalt phthalocyanine

from MedChemExpress
HY-18761 | 1g: 119.00 EUR

Cobalt(Ii) Oxide

from Abbexa
abx188657-25g | 25 g: 314.00 EUR

Cobalt(Iii) Fluoride

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abx188658-25g | 25 g: 370.00 EUR

High Density Cobalt

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6BCL-QHCo-100 | 100 ml: 372.00 EUR

High Density Cobalt

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6BCL-QHCo-25 | 25 ml: 162.00 EUR

High Density Cobalt

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6BCL-QHCo-500 | 500 ml: 1304.00 EUR

Cobalt Rapid Run

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6CoRR-100 | 100 ml: 431.00 EUR

Cobalt Rapid Run

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6CoRR-25 | 25 ml: 166.00 EUR

Cobalt Rapid Run

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6CoRR-500 | 500 ml: 1474.00 EUR

Cobalt Assay Kit

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55R-1435 | 100 assays: 621.00 EUR

Cobalt(II) acetate tetrahydrate

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GK1133-100G | 100 g: 48.00 EUR
The sodium cation (site symmetry ), has a single water mol-ecule bound to it in the asymmetric unit and yields a distorted, octa-hedrally coordinated hydrated [Na(H2O)6]+ cation after the application of symmetry. One of the chloride ions lies on a general position and the other has site symmetry. An extensive array of C-HO, N-HCl and O-HCl hydrogen bonds exists between the ethyl-ene di-amine ligands, the water mol-ecules of hydration, and the anions present, thereby furnishing solid-state stability.
Keywords: crystal structure; enanti­omer; ethyl­ene di­amine; racemate.