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. 2017 Aug 18;7:8837. doi: 10.1038/s41598-017-08879-x

Figure 2.

Figure 2

Liver on a chip: On-chip response to acetaminophen, N-acetyl-L-cysteine countermeasure. (a) A depiction of the liver-on-a-chip microreactor device. (b–e) Liver organoids respond to acetaminophen toxicity and are rescued by NAC. Viability as determined by LIVE/DEAD staining on day 14. Organoids were exposed to (b) a 0 mM APAP control, (c) 1 mM APAP, (d) 10 mM APAP, or (e) 10 mM APAP with 20 mM N-acetyl-L-cysteine. Green – Calcein AM-stained viable cells; Red – Ethidium homodimer-stained dead cells. (f–i) Analysis of media aliquots indicate that APAP induces loss of function and cell death, while NAC has the capability to mitigate these negative effects. Only 10 mM APAP treatment data shown. Quantification of (f) human albumin, (g) urea, (h) lactate dehydrogenase, and (i) alpha-GST. Albumin and urea output are negatively effected by APAP treatments, while NAC decreases this reduction in secretion. LDH and alph-GST are low in control and APAP + NAC groups demonstrating functional cells, while APAP induces elevated levels, indicating apoptosis and release of LDH and alpha-GST into the media. Statistical significance: *p < 0.05 between control and APAP; #p < 0.05 APAP + NAC and APAP.