Briggs D W, Condie L W, Sedman R M, Tephly T R
J Biol Chem. 1976 Aug 25;251(16):4996-5001.
The regultion of cardiac delta-aminolevulinic acid synthetase activity was studied in rat heart homogenates. Optimal conditions were determined for the measurement of delta-aminolevulinic acid and an appropriate assay was established for the heart. The activity of cardiac delta-aminolevulinic acid synthetase was determined in rats either fed ad libitum or starved for 24 or 48 h. Marked decreases in delta-aminolevulinic acid synthetase activity were observed in homogenates or mitochondrial fractions prepared from hearts of fasted animals and an explanation for previous findings that the enzyme is undetectable in heart tissue is provided. Dexamethasone treatment was effective in reversing the decreases brought about by fasting but had no effect on the delta-aminolevulinic acid synthetase activity in heart homogenates from fed rats. ACTH treatment had no effect in fed or starved rats. Decreases in delta-aminolevulinic acid synthetase activity induced by fasting were not reversed in homogenates or mitochondrial preparations by succinyl-CoA-generating systems or when alpha-ketoglutarate was substituted for succinate in homogenate preparations. Cardiac delta-aminolevulinic acid dehydratase levels are not altered by fasting. Agents such as allylisopropylacetamide or 3,5-dicarbethoxy-1,4-dihydrocollidine, which produce marked increases in hepatic delta-aminolevulinic acid synthetase activity, have no effects on the activity of this enzyme in the heart.
在大鼠心脏匀浆中研究了心脏δ-氨基-γ-酮戊酸合成酶活性的调节。确定了测量δ-氨基-γ-酮戊酸的最佳条件,并建立了适合心脏的检测方法。测定了随意进食、饥饿24小时或48小时大鼠心脏中δ-氨基-γ-酮戊酸合成酶的活性。在禁食动物心脏制备的匀浆或线粒体组分中观察到δ-氨基-γ-酮戊酸合成酶活性显著降低,并对先前在心脏组织中未检测到该酶的发现提供了解释。地塞米松治疗可有效逆转禁食引起的活性降低,但对进食大鼠心脏匀浆中的δ-氨基-γ-酮戊酸合成酶活性没有影响。促肾上腺皮质激素治疗对进食或饥饿大鼠均无影响。禁食诱导的δ-氨基-γ-酮戊酸合成酶活性降低,在匀浆或线粒体制剂中,通过琥珀酰辅酶A生成系统或在匀浆制剂中用α-酮戊二酸替代琥珀酸时,均未得到逆转。禁食不会改变心脏δ-氨基-γ-酮戊酸脱水酶水平。能使肝脏δ-氨基-γ-酮戊酸合成酶活性显著增加的药物,如烯丙异丙基乙酰胺或3,5-二乙氧羰基-1,4-二氢可力丁,对心脏中该酶的活性没有影响。