Enhancement of L-3-hydroxybutyryl-CoA dehydrogenase activity and circulating ketone body levels by pantethine. Relevance to dopaminergic injury

Table 1 Effects of pantethine treatment on L-3-hydroxybutyryl-CoA dehydrogenase activity.

Days after 2'methyl -MPTP injection	L-3-hydroxybutyryl-CoA dehydrogenase activity
	Brain (nmol.min^-1.mg protein^-1)		Liver (μmol.min¹.mg protein^-1)
	Saline	Pantethine	Saline	Pantethine
d0	63.91 ± 4.90	73.95 ± 2.55#	2.96 ± 0.35	3.11 ± 0.27
d1	28.91 ± 3.54**	51.09 ± 4.87##	2.74 ± 0.14	3.56 ± 0.18#
d2	35.58 ± 3.31**	45.82 ± 3.84#	2.08 ± 0.17**	2.94 ± 0.19##
d4	45.01 ± 5.19*	46.01 ± 5.05	1.60 ± 0.27**	2.98 ± 0.32##
d7	54.31 ± 4.95	57.55 ± 3.65	2.67 ± 0.18	2.85 ± 0.17

Brain and liver mitochondria were isolated from 2'-methyl-MPTP- injected mice, previously treated with saline or pantethine. Tissue and blood samples were collected from day 0 to day 7 following the neurotoxin injection and were then processed for dehydrogenase activity, i.e conversion of L-3-hydroxybutytyl-CoA to acetoacetyl-CoA. Values are means ± SD; n = 4 mice per assay. Significant decrease versus d0 control, *p < 0.05 and **p < 0.01; significant increase versus paired saline, #p < 0.05 and ##p < 0.01.

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