scholarly journals Antitumor effects of Camptothecin driveritive CPT-11 on malignant melanom transtable to nude mouse (SK-14 strain).

Skin Cancer ◽  
1990 ◽  
Vol 5 (1) ◽  
pp. 239-248
Author(s):  
Tsutomu KOIDE ◽  
Teruo KOMATSU ◽  
Kazuyuki ISHIHARA
Keyword(s):  
Nude Mouse ◽  
Antitumor Effects

Spontaneous Cataract in Nude Athymic Mice

1977 ◽  
Vol 35 ◽  
pp. 512-513
Author(s):  
Ronald H. Bradley ◽  
R. S. Berk ◽  
L. D. Hazlett
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Nude Mouse ◽  
Cellular Immunity ◽  
Phosphate Buffer ◽  
Osmium Tetroxide ◽  
Athymic Mice ◽  
Transmission Microscopy ◽  
Mouse Lens ◽  
Scanning Electron

The nude mouse is a hairless mutant (homozygous for the mutation nude, nu/nu), which is born lacking a thymus and possesses a severe defect in cellular immunity. Spontaneous unilateral cataractous lesions were noted (during ocular examination using a stereomicroscope at 40X) in 14 of a series of 60 animals (20%). This transmission and scanning microscopic study characterizes the morphology of this cataract and contrasts these data with normal nude mouse lens.All animals were sacrificed by an ether overdose. Eyes were enucleated and immersed in a mixed fixative (1% osmium tetroxide and 6% glutaraldehyde in Sorenson's phosphate buffer pH 7.4 at 0-4°C) for 3 hours, dehydrated in graded ethanols and embedded in Epon-Araldite for transmission microscopy. Specimens for scanning electron microscopy were fixed similarly, dehydrated in graded ethanols, then to graded changes of Freon 113 and ethanol to 100% Freon 113 and critically point dried in a Bomar critical point dryer using Freon 13 as the transition fluid.

Mitochondria: the birth place, battle ground and the site of melatonin metabolism in cells

2019 ◽  
Vol 2 (1) ◽  
pp. 44-66 ◽  
Author(s):  
Dun-Xian Tan ◽  
Russel. J. Reiter
Keyword(s):  
Ischemia Reperfusion ◽  
Surface Membrane ◽  
Strong Association ◽  
Membrane Receptors ◽  
Melatonin Receptors ◽  
Metabolic Enzyme ◽  
Intermembrane Space ◽  
Antitumor Effects ◽  
The Matrix ◽  
Surprising Discovery

     It was a surprising discovery when mitochondria, as the power houses of cells, were also found to synthesize the potent mitochondrial targeted antioxidant, melatonin. The melatonin synthetic enzyme serotonin N-acetyltransferase (SNAT) was found in matrix and also in the intermembrane space of mitochondria. We hypothesize that the melatonin synthesis occurs in the matrix due to substrate (N-acetyl co-enzyme A) availability while the intermembrane space may serve as the recycling pool of SNAT to regulate the melatonin circadian rhythm. Another surprise was that the melatonin membrane receptors, including MT1 and MT2, were also present in mitochondria. The protective effects of melatonin against neuronal injury induced by brain ischemia/reperfusion were proven to be mainly mediated by mitochondrial melatonin receptors rather than the cell surface membrane receptors which is contrary to the classical principle. In addition, melatonin metabolic enzyme has also been identified in the mitochondria. This enzyme can convert melatonin to N-acetylserotonin to strengthen the antitumor effects of melatonin. Thus, mitochondria are the generator, battle ground and metabolic sites of melatonin. The biological significance of the strong association between mitochondria and melatonin should be intensively investigated. 

Mitochondria: the birth place, battle ground and the site of melatonin metabolism in cells

2019 ◽  
Vol 2 (1) ◽  
pp. 44-66 ◽  
Author(s):  
Dun-Xian Tan ◽  
Russel. J. Reiter
Keyword(s):  
Ischemia Reperfusion ◽  
Surface Membrane ◽  
Strong Association ◽  
Membrane Receptors ◽  
Melatonin Receptors ◽  
Metabolic Enzyme ◽  
Intermembrane Space ◽  
Antitumor Effects ◽  
The Matrix ◽  
Surprising Discovery

     It was a surprising discovery when mitochondria, as the power houses of cells, were also found to synthesize the potent mitochondrial targeted antioxidant, melatonin. The melatonin synthetic enzyme serotonin N-acetyltransferase (SNAT) was found in matrix and also in the intermembrane space of mitochondria. We hypothesize that the melatonin synthesis occurs in the matrix due to substrate (N-acetyl co-enzyme A) availability while the intermembrane space may serve as the recycling pool of SNAT to regulate the melatonin circadian rhythm. Another surprise was that the melatonin membrane receptors, including MT1 and MT2, were also present in mitochondria. The protective effects of melatonin against neuronal injury induced by brain ischemia/reperfusion were proven to be mainly mediated by mitochondrial melatonin receptors rather than the cell surface membrane receptors which is contrary to the classical principle. In addition, melatonin metabolic enzyme has also been identified in the mitochondria. This enzyme can convert melatonin to N-acetylserotonin to strengthen the antitumor effects of melatonin. Thus, mitochondria are the generator, battle ground and metabolic sites of melatonin. The biological significance of the strong association between mitochondria and melatonin should be intensively investigated. 

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