N-Methyl-d-Aspartate Receptor and Neuronal Nitric Oxide Synthase Activation Mediate Bilirubin-Induced Neurotoxicity

Table 1 MK-801 abrogates UCB-induced nNOS overexpression, nitrite formation, cGMP production, MTT reduction impairment and LDH release, but not extracellular glutamate accumulation.^a

	Control	UCB	MK-801	UCB + MK-801
Glutamate, µmol/L	7.02 ± 0.76	130.12 ± 5.54^b	6.39 ± 0.69	121.71 ± 5.76
nNOS, fold change	1.00 ± 0.00	1.98 ± 0.36^b	1.04 ± 0.12	1.13 ± 0.23^c
Nitrite, µmol/L	0.39 ± 0.10	0.94 ± 0.12^b	0.49 ± 0.08	0.39 ± 0.08^d
cGMP, pmol/mg protein	13.49 ± 1 . 46	22.58 ± 1 .89^b	15.88 ± 1.41	15.39 ± 2.03^c
mtt, %	100 ± 0.00	46.82 ± 1.28^b	90.45 ± 4.89	64.99 ± 3.93^b,d
LDH, %	3.66 ± 0.75	8.55 ± 0.80^b	3.89 ± 0.75	3.29 ± 1.10^d

^aRat neurons in primary culture were treated for 4 h at 37°C with 100 µmol/L UCB, 1 µmol/L MK-801, UCB plus MK-801, or no addition (control), in the presence of 100 µmol/L HSA. Determinations of nNOS expression, as well as of nitrite, cGMP LDH and glutamate levels, and MTT reduction test were performed as described in Materials and Methods.
^bP< 0.01 from control.
^cP< 0.05 and ^dP< 0.01 from UCB.

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