Prolongation of life in an experimental model of aging in Drosophila melanogaster

被引:44
作者
Jordens, RG
Berry, MD
Gillott, C
Boulton, AA
机构
[1] Univ Saskatchewan, Neuropsychiat Res Unit, Saskatoon, SK S7N 5E4, Canada
[2] Univ Saskatchewan, Dept Biol, Saskatoon, SK S7N 5E4, Canada
关键词
Drosophila melanogaster; galactose; aging model; superoxide dismutase; knock-out mutant; (R)-deprenyl; aliphatic propargylamines;
D O I
10.1023/A:1022510004220
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
(R)-Deprenyl, the archetypical monoamine oxidase-B inhibitor, has been shown to increase lifespan in a number of species. Although many theories for this effect have been suggested, for example, an increase in superoxide dismutase (SOD) activity, the mechanism of action has yet to be elucidated. To investigate this phenomenon, we have examined the effects of (R)-deprenyl, and some aliphatic propargylamines, in an experimental aging model in Drosophila melanogaster. Both wild-type Oregon-R type flies, as well as a SOD knock-out mutant strain were used. Flies obtained from a series of paired mates were divided equally among treatment groups. In all studies, flies were treated for the duration of life following adult emergence. The aging model consists of substitution of sucrose with galactose in the regular food media of the flies. Initial experiments con-firmed that such a substitution resulted in a significant (p < 0.01, Breslow test) reduction in mean and maximal life-span of flies, an effect not due to nutrient deprivation. Inclusion of (R)deprenyl and the aliphatic propargylamines in the media, at average daily doses in the range 0.5-1ng/fly/day, led to a significant increase in mean and maximal life-span of galactose-treated, but not control flies. This effect was seen in both wild-type and mutant flies.
引用
收藏
页码:227 / 233
页数:7
相关论文
共 54 条
[1]
POSSIBLE MECHANISMS OF ACTION OF (-)DEPRENYL AND OTHER MAO-B INHIBITORS IN SOME NEUROLOGIC AND PSYCHIATRIC-DISORDERS [J].
BERRY, MD ;
JUORIO, AV ;
PATERSON, IA .
PROGRESS IN NEUROBIOLOGY, 1994, 44 (02) :141-161
[2]
BERRY MD, 1997, J NEUROCHEM, V69, pS168C
[3]
POTENTIATION OF ANTI AKINETIC EFFECT AFTER L-DOPA TREATMENT BY AN INHIBITOR OF MAO-B, DEPRENIL [J].
BIRKMAYER, W ;
RIEDERER, P ;
YOUDIM, MBH ;
LINAUER, W .
JOURNAL OF NEURAL TRANSMISSION, 1975, 36 (3-4) :303-326
[4]
BIRLOUEZARAGON I, 1993, J NUTR, V123, P1370
[5]
Boulton A A, 1998, Adv Pharmacol, V42, P308
[6]
Boulton AA, 1997, DRUG DEVELOP RES, V42, P150, DOI 10.1002/(SICI)1098-2299(199711/12)42:3/4<150::AID-DDR6>3.0.CO
[7]
2-P
[8]
COEXISTENCE OF NERVE-CONDUCTION DEFICIT WITH INCREASED NA+-K+-ATPASE ACTIVITY IN GALACTOSE-FED MICE - IMPLICATIONS FOR POLYOL PATHWAY AND DIABETIC NEUROPATHY [J].
CALCUTT, NA ;
TOMLINSON, DR ;
BISWAS, S .
DIABETES, 1990, 39 (06) :663-666
[9]
(-) DEPRENYL INDUCES ACTIVITIES OF BOTH SUPEROXIDE-DISMUTASE AND CATALASE BUT NOT OF GLUTATHIONE-PEROXIDASE IN THE STRIATUM OF YOUNG MALE-RATS [J].
CARRILLO, MC ;
KANAI, S ;
NOKUBO, M ;
KITANI, K .
LIFE SCIENCES, 1991, 48 (06) :517-521
[10]
(-)-DEPRENYL CAN INDUCE SOLUBLE SUPEROXIDE-DISMUTASE IN RAT STRIATA [J].
CLOW, A ;
HUSSAIN, T ;
GLOVER, V ;
SANDLER, M ;
DEXTER, DT ;
WALKER, M .
JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION, 1991, 86 (01) :77-80