ABSTRACT
BACKGROUND: Cancer is one of the leading cause of death worldwide. Besides current therapies and treatments to counter cancer, new alternatives are required to diminish the cell proliferation of oncogenic processes. METHODS: One of the most promissory therapy includes the use of blue scorpion venom as a specific cytotoxic agent to kill tumoral cells, including Glioblastoma multiforme. OBJECTIVES: We show evidence of the cytotoxic effect of blue scorpion venom in a cellular model of Glioblastoma multiforme. RESULTS: Our results demonstrate that 50 µg/ml of scorpion venom is capable to diminish the viability of Glioblastoma populations. CONCLUSION: It is possible that the action mechanism could be associated with a loss of membrane integrity. Additionally, some metalloproteinases as MMP2 and MMP9 may also participate in the potential action mechanism.
Subject(s)
Antineoplastic Agents/pharmacology , Brain Neoplasms/drug therapy , Glioblastoma/drug therapy , Scorpion Venoms/pharmacology , Animals , Cell Line, Tumor , Cell Membrane/drug effects , Cell Survival/drug effects , Humans , ScorpionsABSTRACT
Traumatic Brain Injury is considered one of the most prevalent causes of death around the world; more than seventy millions of individuals sustain the condition per year. The consequences of traumatic brain injury on brain tissue are complex and multifactorial, hence, the current palliative treatments are limited to improve patients' quality of life. The subsequent hemorrhage caused by trauma and the ongoing oxidative process generated by biochemical disturbances in the in the brain tissue may increase iron levels and reactive oxygen species. The relationship between oxidative damage and the traumatic brain injury is well known, for that reason, diminishing factors that potentiate the production of reactive oxygen species have a promissory therapeutic use. Iron chelators are molecules capable of scavenging the oxidative damage from the brain tissue and are currently in use for ironoverload- derived diseases. Here, we show an updated overview of the underlying mechanisms of the oxidative damage after traumatic brain injury. Later, we introduced the potential use of iron chelators as neuroprotective compounds for traumatic brain injury, highlighting the action mechanisms of iron chelators and their current clinical applications.
