Applying fiber optical methods for toxicological testing in vitro

Maerz, Holger K.; Emmrich, Frank; Fink, F. N.; Geddes, Clive L.; Raabe, F; Scheper, T.; Ulrich, Elizabeth; Marx, Uwe

doi:10.1117/12.346746

Cited by 2 publications

(1 citation statement)

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“…Reported biotechnologies for measuring dissolved oxygen include: ( 1 ) Electrochemical sensors (Clark electrodes, polarographic or Galvanic) that generate electrical signals in response to oxygen reduction by the polarized electrode [ 12 ]; ( 2 ) Optical sensors based on oxygen quenching fluorescence [ 13 , 14 , 15 ], phosphorescence [ 16 , 17 , 18 ], or luminescence; and ( 3 ) Micro-electrochemical techniques (scanning electrochemical microscopy) based on measurements of flow of small molecules, such as oxygen in tissues [ 19 ]. The use of ‘fluorophore-based biosensors, including solid state cartridges’ [ 20 , 21 , 22 ] and ‘high-resolution FluoRespirometry’ [ 14 ] have become relatively popular.…”

Section: Introductionmentioning

confidence: 99%

Conserved spinal cord bioenergetics in experimental autoimmune encephalomyelitis in C57BL6 mice, measured using phosphorescence oxygen analyzer

Shamsi

Shahin

Kamyan

et al. 2021

Heliyon

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Background: We have previously reported that spinal cord respiration (cellular mitochondrial oxygen consumption) and ATP content are conserved in the studied model of experimental autoimmune encephalomyelitis (EAE), foreseeing a recovery of the diseased rats. This exemplary lesion of multiple sclerosis is used here to measure spinal cord bioenergetics in C57BL6 mice. Our hypothesis is that, despite the well-known focal axonal mitochondrial pathology, bioenergetics of the CNS is reasonably preserved in this disease. Methods: EAE was induced with an immunodominant myelin oligodendrocyte glycoprotein epitope in complete Freund's adjuvant, appended by injections of pertussis toxin. A low-and high-dose of the encephalitogen, administered into base of tail or hind-flank, were investigated. Control mice received only the incomplete adjuvant into tail. Oxygen measurements were based on quenching the phosphorescence of Pd(II) meso-tetra (sulfophenyl) tetrabenzoporphyrin by molecular oxygen. Cellular ATP was measured using the luciferin/luciferase system. Results: The kinetics of spinal cord oxygen consumption was zero-order (linear with time) and inhibited by cyanide, confirming oxygen was reduced by cytochrome oxidase. The rate of respiration (in μM O 2 .min À1 .mg À1 ; measured on Days 13-28) in control mice was (mean AE SD) 0.086 AE 0.024 (n ¼ 8) and in immunized mice was 0.079 AE 0.020 (n ¼ 15, P ¼ 0.265, Mann-Whitney test). Consistently, cellular ATP (in μmol mg À1 dry pellet weight; measured on Days 13-28) in control mice was 0.068 AE 0.079 (n ¼ 11) and in immunized mice was 0.063 AE 0.061 (n ¼ 24, P ¼ 0.887, Mann-Whitney U test). Conclusions: In vitro measurements of spinal cord bioenergetics show conservation of the mitochondrial function in mice with EAE. These results suggest the previously documented reduced mitochondrial electrochemical potential in this disease is alterable, and likely reflects the adverse events of neuroinflammation.

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