The resist apoptotic cell death[24]. Acute myeloid leukemia

The induction of apoptosis is offered
to be an impressive strategy for treatment of cancer, since, cell numbers are related
to the amount of cell proliferation and death. However, malignant cells have
developed several mechanisms to resist apoptotic cell death24. Acute myeloid leukemia (AML) is a Heterogeneous  hematologic malignancy
characterized by the clonal expansion of immature myeloid blasts25. LSCs are a subpopulation of leukemic cells that indicate characteristics
of self-renewal, tumor-initiating and differentiation capacity. They are also
thought to be responsible for chemotherapy and radiotherapy resistance and the relapse
of leukemia26.There are several documents that exhibit thiosemicarbazones and
their metal complexes might be efficient in the treatment of some diseases such
as cancers27-35. The
antiproliferative effects of TSC were once particularly ascribed to the
inhibition of ribonucleotide reductase enzyme that is involved in the step of rate-limiting the synthesis
of DNA. However, the mechanism of this inhibition was initially not
demonstrated. The capability of thiosemicarbazones to chelate metal ions has
now been recognized as the main agent in their antiproliferative properties. For example, The redox activity of
Fe–thiosemicarbazone complexes is significant in their antitumor
effects, resulting in oxidative damage and the inhibition of ribonucleotide
reductase. In vivo studies demonstrate that some thiosemicarbazones indicate
potential as chemotherapeutic factors27.

The attributes
of thiosemicarbazones and their metal complexes have indicated their
adaptability to a range of applications, making them useful molecules for
further assessment as novel potential therapeutic factors aimed at cancer
therapy36. This compound has shown potent anti-proliferative and cytotoxic activities
in several human tumors, Contains A549(human lung adenocarcinoma cell line), K562, U937 (human leukemia
cell line), ECV304 (human umbilical vein endothelial cell line)11, 12, 35, 37. In a study, The antioxidant effects of the Ni–thiosemicarbazone
was investigated to test their free-radical scavenging capability. These
compounds overcome cisplatin resistance in the A549 cells and they were also
active in the HepG2 cells38.

this study, we hypothesized that 4 -HBTC might exert oxidative stress
situations-induced apoptosis in KG1a human cancer cell line. Therefore, we have confirmed the existence of intracellular
reactive oxygen species (ROS) and of lipidic peroxidation in KG1a cells as a
consequence of treatment with nickel thiosemicarbazones. The primary ROS and TBARS increase caused by 4 –HBTC  seem to be limited by the activities of GSH and antioxidant enzymes. Amazingly
these intracellular scavengers seem to have no protective effects on oxidative
stress damages of 4 –HBTC, most amazingly due to Impressive
effects on cellular

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