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Rheumatology Advance Access originally published online on
November 22, 2005 Rheumatology 2006 45(3):287-290;
doi:10.1093/rheumatology/kei149 Experimental Arthritis
=A9 The Author 2005. Published by Oxford University Press on
behalf of the British Society for Rheumatology. All rights
reserved. For Permissions, please email:
journals.permissions@oxfordjournals.org
Oxidative stress by glutathione depletion induces
osteonecrosis in rats
T=2E Ichiseki, Y. Ueda1, S. Katsuda1, K. Kitamura, A. Kaneuji
and T. Matsumoto Department of Orthopaedic Surgery and 1
Department of Pathophysiological and Experimental Pathology,
Kanazawa Medical University, Ishikawa, Japan.
Correspondence to: T. Ichiseki, Department of Orthopaedic
Surgery, Kanazawa Medical University, Daigaku 1-1,
Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan. E-mail:
tsy-ichi@kanazawa-med.ac.jp
Objective. We recently implicated in vivo oxidative stress in
the development of osteonecrosis in a steroid-induced
osteonecrosis model in the domestic rabbit. In the present
experiment we devised a new non-traumatic model using the rat
to investigate the relationship between oxidative stress and
the development of osteonecrosis.
Methods. Seven 24-week-old male Wistar rats were
subcutaneously injected with the pro-oxidant buthionine
sulphoximine (BSO) 500 mg/kg for 14 consecutive days (group B)
and eight rats received injections of vehicle (physiological
saline; group N). The rats in both groups were killed after 14
days, and their bilateral femurs were examined
histopathologically. Blood levels of reduced glutathione
(GSH), total cholesterol (T-cho) and triglycerides (TG) were
also determined.
Results. GSH was significantly decreased in group B
compared with group N (P<0.01). No significant differences
were found in T-cho or TG. Osteonecrosis was not detected
in any animal in group N in contrast to five of seven
animals in group B (P<0.05).
Conclusion. BSO is an inducer of oxidative stress, in
particular interfering with the synthesis of GSH in vivo. In
the present study, GSH levels were markedly reduced by BSO,
whereas neither T-cho nor TG was significantly changed. The
high rate of osteonecrosis noted in group B suggests that
oxidative stress alone may be sufficient to promote the
development of osteonecrosis at certain sites.
KEY WORDS: Osteonecrosis, Oxidative stress, Rat, Glutathione
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING=20 http://tinyurl.com/zk9fk
November 22, 2005 Rheumatology 2006 45(3):287-290;
doi:10.1093/rheumatology/kei149 Experimental Arthritis
=A9 The Author 2005. Published by Oxford University Press on
behalf of the British Society for Rheumatology. All rights
reserved. For Permissions, please email:
journals.permissions@oxfordjournals.org
Oxidative stress by glutathione depletion induces
osteonecrosis in rats
T=2E Ichiseki, Y. Ueda1, S. Katsuda1, K. Kitamura, A. Kaneuji
and T. Matsumoto Department of Orthopaedic Surgery and 1
Department of Pathophysiological and Experimental Pathology,
Kanazawa Medical University, Ishikawa, Japan.
Correspondence to: T. Ichiseki, Department of Orthopaedic
Surgery, Kanazawa Medical University, Daigaku 1-1,
Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan. E-mail:
tsy-ichi@kanazawa-med.ac.jp
Objective. We recently implicated in vivo oxidative stress in
the development of osteonecrosis in a steroid-induced
osteonecrosis model in the domestic rabbit. In the present
experiment we devised a new non-traumatic model using the rat
to investigate the relationship between oxidative stress and
the development of osteonecrosis.
Methods. Seven 24-week-old male Wistar rats were
subcutaneously injected with the pro-oxidant buthionine
sulphoximine (BSO) 500 mg/kg for 14 consecutive days (group B)
and eight rats received injections of vehicle (physiological
saline; group N). The rats in both groups were killed after 14
days, and their bilateral femurs were examined
histopathologically. Blood levels of reduced glutathione
(GSH), total cholesterol (T-cho) and triglycerides (TG) were
also determined.
Results. GSH was significantly decreased in group B
compared with group N (P<0.01). No significant differences
were found in T-cho or TG. Osteonecrosis was not detected
in any animal in group N in contrast to five of seven
animals in group B (P<0.05).
Conclusion. BSO is an inducer of oxidative stress, in
particular interfering with the synthesis of GSH in vivo. In
the present study, GSH levels were markedly reduced by BSO,
whereas neither T-cho nor TG was significantly changed. The
high rate of osteonecrosis noted in group B suggests that
oxidative stress alone may be sufficient to promote the
development of osteonecrosis at certain sites.
KEY WORDS: Osteonecrosis, Oxidative stress, Rat, Glutathione
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING=20 http://tinyurl.com/zk9fk