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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: L- and D-lactate enhance DNA repair and modulate the resistance of cervical carcinoma cells to anticancer drugs via histone deacetylase inhibition and hydroxycarboxylic acid receptor 1 activation

Fig. 2

L- and D-lactate treatment increases DSB repair in cells treated with chemotherapeutics. HeLa cells were incubated in the presence or absence of 20 mM L- or D-lactate for 24 h, followed by treatment with NCS, DOX or CDDP for 30 min. Then, the cells were allowed to recover for the indicated period. a, b, c γ-H2AX foci resolution kinetics after chemotherapeutic treatment (2 nM NCS, 2 μM DOX or 20 μM CDDP). The graphs show the mean number of γ-H2AX foci per cell ± SEM from at least three independent experiments; drug alone (white circles), L-lactate + drug (black square), D-lactate + drug (black triangles). d, e, f DDR dynamics after chemotherapeutic treatment (5 nM NCS, 2 μM DOX or 20 μM CDDP) as measured by a neutral comet assay. The basal Olive tail moment (OTM) was subtracted, and the value observed at 0 h was set to 100 %. The graph shows the mean OTM (% of control) ± SEM from three independent experiments; drug alone (white circles), L-lactate + drug (black square), D-lactate + drug (black triangles)

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