Author/Authors :
Noguti, Juliana Departments of Pathology - Federal University of São Paulo - UNIFESP, Brazil , Aparecida Alvarenga, Tathiana Departments of Psichobiology - Federal University of São Paulo - UNIFESP, Brazil , Levy Andersen, Mônica Departments of Psichobiology - Federal University of São Paulo - UNIFESP, Brazil , Tufik, Sergio Departments of Psichobiology - Federal University of São Paulo - UNIFESP, Brazil , Tijuko Fujiyama Oshima, Celina Departments of Psichobiology - Federal University of São Paulo - UNIFESP, Brazil , Araki Ribeiro, Daniel Departments of Pathology - Federal University of São Paulo - UNIFESP, Brazil
Abstract :
Background: The aim of this study was to evaluate whether paradoxical sleep deprivation could
affects the mechanisms and pathways essentials for cancer cells in tongue cancer induced by
4‑nitroquinole 1‑oxide in Wistar rats.
Materials and Methods: For this purpose, the animals were distributed into 4 groups of 5 animals
each treated with 50 ppm 4 nitroquinoline 1 oxide (4 NQO) solution through their drinking
water for 4 and 12 weeks. The animals were submitted to paradoxical sleep deprivation (PSD)
for 72 h using the modified multiple platform method, which consisted of placing 5 mice in a
cage (41 × 34 × 16 cm) containing 10 circular platforms (3.5 cm in diameter) with water 1 cm
below the upper surface. The investigations were conducted using immunohistochemistry of p53,
Bax and Bcl‑2 proteins related to apoptosis and its pathways. Statistical analysis was performed
by Kruskal‑Wallis non‑parametric test followed by the Dunn’s test using SPSS software pack
(version 1.0). P value < 0.05 was considered for statistic significance.
Results: Although no histopathological abnormalities were induced in the epithelium after 4 weeks
of carcinogen exposure in all groups, in 12 weeks were observed pre‑neoplasic lesions. Data analysis
revealed statistically significant differences (P < 0.05) in 4 weeks group for p53 and for bcl‑2 and
for all immunomarkers after 12 weeks of 4NQO administration.
Conclusion: Our results reveal that sleep deprivation exerted alterations in proteins associated
with proliferation and apoptosis in carcinogenesis.
Keywords :
Apoptosis , carcinogenesis , rat , sleep deprivation