2008
DOI: 10.1111/j.1365-2184.2008.00530.x
|View full text |Cite
|
Sign up to set email alerts
|

Cell proliferation, apoptosis and mitochondrial damage in rat B50 neuronal cells after cisplatin treatment

Abstract: CisPt exerts cytotoxic effects in the neuronal B50 cell line via a caspase-dependent pathway with mitochondria being central relay stations.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

1
29
0

Year Published

2008
2008
2020
2020

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 37 publications
(30 citation statements)
references
References 66 publications
1
29
0
Order By: Relevance
“…It is possible that variation in the endogenous balance between actin monomers and polymers may modulate the signaling to apoptosis, with alterations to actin providing the sensory mechanism [37]. Previous results by our group [3,38,39] demonstrate that different apoptogenic stimuli that do not directly affect the actin status are able to induce similar reorganization of the microfilament cytoskeleton, suggesting that these structural rearrangements may be viewed as an early morphological sign of apoptosis.…”
Section: Resultsmentioning
confidence: 99%
“…It is possible that variation in the endogenous balance between actin monomers and polymers may modulate the signaling to apoptosis, with alterations to actin providing the sensory mechanism [37]. Previous results by our group [3,38,39] demonstrate that different apoptogenic stimuli that do not directly affect the actin status are able to induce similar reorganization of the microfilament cytoskeleton, suggesting that these structural rearrangements may be viewed as an early morphological sign of apoptosis.…”
Section: Resultsmentioning
confidence: 99%
“…Apoptosis of primary sensory dorsal root ganglion (DRG) neurons due to formation of platinum adducts in nuclear and mitochondrial DNA is a central mechanism in rodent models [11-19]. This results in mitochondrial dysfunction and disruption in cell cycle [14, 15, 19]. Thus the mechanisms of neurotoxicity and cancer cytotoxicity have many similarities and separating the beneficial cytotoxic effect from the neurotoxic effect may be difficult.…”
Section: Introductionmentioning
confidence: 99%
“…1 Its serious adverse effects, especially nephrotoxicity, limit high-dose therapy with CP. CP induces renal tubular dysfunction and leads to acute renal injury (AKI) in a large proportion of patients.…”
Section: Introductionmentioning
confidence: 99%