Title:A Newly Synthetized Ferrocenyl Derivative Selectively Induces Apoptosis in ALL Lymphocytes through Mitochondrial Estrogen Receptors
VOLUME: 18 ISSUE: 7
Author(s):Marjan Aghvami, Jalal Pourahmad*, Afshin Zarghi*, Peyman Eshghi, Mohammad H. Zarei, Shabnam Farzaneh and Fatemeh Sattari
Affiliation:Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Pediatric Congenital Hematologic Disorders Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Faculty of Pharmacy, ShahidBeheshti University of Medical Sciences, Tehran, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Pediatric Congenital Hematologic Disorders Research Center, Shahid Beheshti University of Medical Sciences, Tehran
Keywords:Estrogen, ferrocenyl derivative, mitochondrial receptors, apoptosis, acute lymphocytic leukemia, pediatric malignity.
Abstract:Background: Estrogens, as the main female steroid hormones have multiple proven effects on reproductive
and non- reproductive systems. Expression of ERα and ERβ, two dominant estrogen receptors, in peripheral
blood mononuclear cells in certain B-cell malignancies and the existence of estrogens receptors on
mitochondria is open to question that estrogen likely has an impact on the cancerous lymphocytes life span.
Acute Lymphoblastic Leukemia (ALL) is the frequent pediatric malignity which is recurrent and hardly curable
in many cases. The malignant cells are generally resistant to apoptosis caused the severe lymphocytes accumulation
in the peripheral blood.
Methods: By focusing on mitochondria as a life/death center of the cell; in the current research we compared
cytotoxicity effects of a new ferrocenyl derivative with raloxifene as well-known SERMs considering the apoptotic
process and survival of cancerous lymphocytes.
Results: We demonstrated that both ferrocenyl derivative and raloxifene could cause mitochondrial lesion and
initiate the apoptosis process by caspase activation and cytochrome c release.
Conclusion: In brief, the ferrocenyl derivative could induce estrogen-related selective apoptosis on cancerous
lymphocytes by affecting mitochondrial receptors.
