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Tomasz Zarnowski, Maria Tulidowicz, Tomasz Choragiewicz, Rejdak Robert, Tomasz Kocki, Waldemar Andrzej Turski; The Effect Of Ketone Bodies On The Synthesis Of Kynurenic Acid In Bovine Retinal Slices. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6413.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate neuroprotective properties of the ketone bodies acetoacetate (ACA) and β-hydroxybutyrate (BHB) on the synthesis of kynurenic acid (KYNA) in bovine retinal slices through glutamate ionotropic receptor agonists: glutamate (GLU), N-methyl-D-aspartic acid (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and kainic acid (KA).
Quantitative analysis of newly synthesized KYNA was carried out using an HPLC system and detected fluorimetrically. For HPLC measurements of KYNA production, bovine retinal slices were incubated with different concentrations of ketone bodies: ACA or BHB and glutamate receptor agonists: GLU, NMDA, AMPA and KA.
The 1 mM concentration of each of the two ketone bodies: ACA and BHB had no or little influence on the synthesis of KYNA in the bovine retina (99%, p>0,05 and 123%, p<0,05, respectively U Mann-Whitney). At a 3 mM concentration they managed to increase the synthesis to 121%, (p<0,05) and 137%, (p<0,05), respectively.De novo KYNA production in bovine retinal slices was reduced by. KA, GLU, AMPA and NMDA at the concentrations of 1 mM by 57%, 47%, 45% and 32%, respectively, (p<0,05). De novo KYNA production in bovine retinal slices was reduced by. KA, GLU, NMDA and AMPA at the concentrations of 3 mM by 67%, 65%, 58% and 56%, respectively, (p<0,05).ACA and BHB attenuated this effect significantly. KYNA production in the presence of ACA was significantly higher (153%, 83%, 73% and 70% higher, respectively p<0.05), than in those with GLU, NMDA, AMPA and KA alone, KYNA production in the presence of BHB was significantly higher 146%, 130%, 107% and 94% higher, respectively p<0.05), than in those with GLU, KA, AMPA and NMDA alone.
According to the results, it seems that ketone bodies: ACA and BHB may exert their neuroprotective effects by attenuating the glutamate receptor agonists: GLU, NMDA, AMPA or KA. induced reduction of KYNA production. Perhaps increasing the amount of ketone bodies in the retina may prevent its neurodegeneration caused by excitotoxicity.
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