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, O-2(-), 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 CoCl(2)(-)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.

Automated summary

This study evaluated the potential mechanism of microbe-derived antioxidants (MA) fermented by probiotics in attenuating cobalt chloride (CoCl2)-induced toxicology in buffalo rat liver cells. The results showed that MA had high antioxidant activity and could mitigate CoCl2-induced cell apoptosis and mitochondrial dysfunction. These findings provide promising constituents for reducing cobalt-induced toxicity in functional foods.