Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...

More documents

Recommendations

Info

CHAPTER 1 RESULTS Effects of 6-OHDA administration on TBARS concentration 92 As shown in Fig. 1, the intrastriatal administration of 6 μg of 6-OHDA in the right striatum caused a significant and progressive increase of TBARS concentration in both right striatum (F(7,24) = 51.73, p < 0.001) and right ventral midbrain (F(7,24) = 72.81, p < 0.001), obtaining a peak-effect 48 h after the injection. Although, the increase in the right striatum was significant at 5 min versus 1 h for ventral midbrain, the augmentation observed after 48 h was higher in the right ventral midbrain (+83%) than in the right striatum (+26%). At 7-day post-injection, the values returned to those of the controls. A significant and progressive increase in the TBARS concentration was also observed in the contralateral side, affecting again to both left striatum (F(7,24) = 10.39, p < 0.001) and left ventral midbrain (F(7,24) = 6.30, p < 0.001). The peak-effect was also observed at 48 h, but the increase was lower (+23% in the left striatum and +26% in the left ventral midbrain). At 7-day post-injection the values returned to the concentrations found in the corresponding controls. Effects of 6-OHDA administration on PCC The PCC also exhibited a significant and progressive time course increase (Fig. 2), which affected both right striatum (F(7,24) = 57.55, p < 0.001) and right ventral midbrain (F(7,24) = 54.76, p < 0.001). In this case, the increase observed in PCC was not significant till 1-h post-injection. However, the peak-effect was observed once again 48 h after injection, and higher in the right ventral midbrain (+42%) than in the right striatum (+38%). A significant and progressive increase in PCC was also observed in the contralateral side, affecting to both left striatum (F(7,24) = 5.95, p < 0.001) and left ventral midbrain (F(7,24) = 3.48, p < 0.05). However, in this case, although the peak- effect was also observed at 48-h post-injection, the increase found was lower (+12% in
CHAPTER 1 the left striatum and +11% in the left ventral midbrain). The corresponding concentrations achieved values close to those found in the controls at 7-day post- injection. Effects of 6-OHDA administration on PTC Figure 3 shows the time-course of the changes observed for PTC in proteins following 6-OHDA administration. As can be seen, a significant and progressive reduction in PTC was found in both right striatum (F(7,24) = 5.06, p < 0.05) and right ventral midbrain (F(7,24) = 25.87, p < 0.001). The maximal decrease for both right striatum (–7%) and right ventral midbrain (–20%) was found at 24 h. Although the peak-effect did not happen at the same time for both TBARS concentration and PCC, the value obtained for PTC at 24 h was not significantly different when compared with that observed 48-h post-injection. The PTC in the contralateral side only exhibited a significant reduction in the left ventral midbrain (F(7,24) = 5.06, p < 0.05), because the changes observed in the left striatum did not reach statistical significance (F(7,24) = 0.87, p > 0.05). Once again, the minimum value found in the left striatum for PTC was observed 24-h post-injection and the decrease was of –8%, a value lower than that found in the ipsilateral side. No significant differences were found when the value obtained at 24 h was compared with that obtained at 48 h. 93
Page 1:
Universidade de Santiago de Compost
Page 5:
Don Ramón Soto Otero y Doña Estef
Page 9 and 10:
Acknowledgements The work of this t
Page 11 and 12:
Abbreviations AA ascorbic acid AD A
Page 13:
Abbreviations (continuation) PCC pr
Page 16 and 17:
List of figures (continuation) Chap
Page 19 and 20:
TABLE OF CONTENTS INTRODUCTION ....
Page 21:
CHAPTER 3 Brain oxidative stress an
Page 25 and 26:
INTRODUCTION PARKINSON’S DISEASE
Page 27 and 28:
INTRODUCTION PD is found in all eth
Page 29 and 30:
Bradykinesia INTRODUCTION Bradykine
Page 31 and 32:
INTRODUCTION predate the occurrence
Page 33 and 34:
Table 1: Differential diagnostic in
Page 35 and 36:
INTRODUCTION Table 3: National Inst
Page 37 and 38:
Figure 4: Dopamine catabolism (Mén
Page 39 and 40:
The basal ganglia INTRODUCTION The
Page 41 and 42:
The death of SNpc DAergic neurons I
Page 43 and 44:
INTRODUCTION the dorsomedial part o
Page 45 and 46:
INTRODUCTION characterized as are l
Page 47 and 48:
INTRODUCTION (Olanow et al. 2004).
Page 49 and 50:
Etiology and pathogenesis of PD INT
Page 51 and 52:
Ageing INTRODUCTION Ageing remains
Page 53 and 54:
INTRODUCTION The finding of MPTP to
Page 55 and 56:
INTRODUCTION may clarify why many n
Page 57 and 58:
Misfolding and aggregation of prote
Page 59 and 60:
INTRODUCTION (E3) (Figure 18A). Los
Page 61 and 62:
INTRODUCTION in connection with Par
Page 63 and 64:
INTRODUCTION Oxidative damage happe
Page 65 and 66: DA metabolism as a source of ROS IN
Page 67 and 68: Contribution of oxidative and nitro
Page 69 and 70: Excitotoxicity INTRODUCTION Glutama
Page 71 and 72: INTRODUCTION al. 1996, Cicchetti et
Page 73 and 74: Experimental models of PD INTRODUCT
Page 75 and 76: INTRODUCTION induce selective DAerg
Page 77 and 78: ALUMINIUM General features INTRODUC
Page 79 and 80: INTRODUCTION Varying amounts of alu
Page 81 and 82: INTRODUCTION and antiperspirants co
Page 83 and 84: INTRODUCTION approximately 3% of al
Page 85 and 86: Excretion INTRODUCTION As insoluble
Page 87 and 88: INTRODUCTION 3.5 mg may be increase
Page 89 and 90: INTRODUCTION Oteiza 1999), non-iron
Page 91 and 92: Aluminium as a cell membrane menace
Page 93 and 94: INTRODUCTION mobilization of Ca 2+
Page 95: Aluminium impairs neurotransmission
Page 99 and 100: AIMS OF THE PRESENT THESIS The main
Page 101: OBJETIVOS
Page 104 and 105: OBJETIVOS 3) Evaluar de forma preci
Page 107: CHAPTER 1 Time-course of brain oxid
Page 110 and 111: CHAPTER 1 INTRODUCTION 86 6-OHDA (2
Page 112 and 113: CHAPTER 1 MATERIALS AND METHODS Che
Page 114 and 115: CHAPTER 1 followed by centrifugatio
Page 118 and 119: CHAPTER 1 DISCUSSION 94 As shown by
Page 120 and 121: CHAPTER 1 strategies or to study th
Page 122 and 123: CHAPTER 1 Fig. 2 Changes in PCC in
Page 125: CHAPTER 2
Page 129 and 130: ABSTRACT CHAPTER 2 In the present w
Page 131 and 132: MATERIALS AND METHODS Chemicals CHA
Page 133 and 134: CHAPTER 2 atomization used were 1,5
Page 135 and 136: DISCUSSION CHAPTER 2 Aluminium ente
Page 137: Table 1. Graphite furnace programme
Page 141: CHAPTER 3 Brain oxidative stress an
Page 144 and 145: CHAPTER 3 INTRODUCTION 120 The huma
Page 146 and 147: CHAPTER 3 MATERIALS AND METHODS Che
Page 148 and 149: CHAPTER 3 1:15 for hippocampus and
Page 150 and 151: CHAPTER 3 initially incorporated to
Page 152 and 153: CHAPTER 3 RESULTS In vivo effects o
Page 154 and 155: CHAPTER 3 Effects of aluminium admi
Page 156 and 157: CHAPTER 3 DISCUSSION 132 Aluminium
Page 158 and 159: CHAPTER 3 hippocampus, showed simil
Page 160 and 161: CHAPTER 3 assume that the distinct
Page 162 and 163: CHAPTER 3 Fig. 1 Levels of TBARS (A
Page 164 and 165: CHAPTER 3 Fig. 2 Enzyme activity of
Page 166 and 167:
CHAPTER 3 Fig. 3 Microphotographs s
Page 168 and 169:
CHAPTER 3 Fig. 5 Levels of TBARS (A
Page 170 and 171:
CHAPTER 3 Fig. 6 In vitro effects o
Page 173:
SUMMARY
Page 176 and 177:
SUMMARY values were attained at 48
Page 178 and 179:
SUMMARY neurodegeneration in the DA
Page 181 and 182:
CONCLUSIONS The results obtained in
Page 183:
13) Aluminium does affect neither M
Page 187 and 188:
RESUMEN RESUMEN Desde el punto de v
Page 189 and 190:
RESUMEN zonas cerebrales excepto en
Page 191:
CONCLUSIONES
Page 194 and 195:
CONCLUSIONES Capítulo 2 4) La admi
Page 196 and 197:
CONCLUSIONES 172 En base a las conc
Page 199 and 200:
Publications as a direct result fro
Page 201:
REFERENCES
Page 204 and 205:
REFERENCES Agil A., Duran R., Barre
Page 206 and 207:
REFERENCES Baquet Z. C., Bickford P
Page 208 and 209:
REFERENCES 184 1,2,3,6-tetrahydropy
Page 210 and 211:
REFERENCES 186 compacta of the subs
Page 212 and 213:
REFERENCES Chung K. K., Dawson V. L
Page 214 and 215:
REFERENCES Davies K. J. (2001) Degr
Page 216 and 217:
REFERENCES Dhillon A. S., Tarbutton
Page 218 and 219:
REFERENCES Ekstrand M. I., Falkenbe
Page 220 and 221:
REFERENCES Fleming S. M., Delville
Page 222 and 223:
REFERENCES Ghribi O., Dewitt D. A.,
Page 224 and 225:
REFERENCES Good P. F., Olanow C. W.
Page 226 and 227:
REFERENCES Hamilton E. I., Miniski
Page 228 and 229:
REFERENCES Hirsch E. C., Brandel J.
Page 230 and 231:
REFERENCES Inden M., Kitamura Y., T
Page 232 and 233:
REFERENCES Johnson V. J. and Sharma
Page 234 and 235:
REFERENCES Kim W. G., Mohney R. P.,
Page 236 and 237:
REFERENCES Kuhn W., Winkel R., Woit
Page 238 and 239:
REFERENCES 214 K.D. and Polymeropou
Page 240 and 241:
REFERENCES Maraganore D. M., Lesnic
Page 242 and 243:
REFERENCES McCord J. M. and Fridovi
Page 244 and 245:
REFERENCES Miu A. C. and Benga O. (
Page 246 and 247:
REFERENCES Nair V. D., McNaught K.,
Page 248 and 249:
REFERENCES Onyango I. G. (2008) Mit
Page 250 and 251:
REFERENCES Perez F. A. and Palmiter
Page 252 and 253:
REFERENCES Przedborski S. and Goldm
Page 254 and 255:
REFERENCES Rifat S. L., Eastwood M.
Page 256 and 257:
REFERENCES Rymar V. V., Sasseville
Page 258 and 259:
REFERENCES Savory J., Herman M. M.
Page 260 and 261:
REFERENCES Shimizu H., Mori T., Koy
Page 262 and 263:
REFERENCES 238 the generation of hy
Page 264 and 265:
REFERENCES Taylor G. A., Moore P. B
Page 266 and 267:
REFERENCES Um J. W., Stichel-Gunkel
Page 268 and 269:
REFERENCES Vila M. and Przedborski
Page 270 and 271:
REFERENCES Whitehead M. W., Farrar
Page 272 and 273:
REFERENCES Yokel R. A. (2002a) Alum
Page 274:
REFERENCES Zhou W., Zhu M., Wilson
show all

Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?