Oxidative stress and apoptotic changes in murine splenocytes exposed to cadmium

Pathak, Neelima; Khandelwal, Shashi

doi:10.1016/j.tox.2005.11.027

Cited by 138 publications

(84 citation statements)

References 43 publications

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“…In a recently documented study, cadmium chloride was reported to induce DNA damage and apoptosis of human liver carcinoma cells via oxidative stress (Skipper et al, 2016). Previous studies carried out in mouse liver by Habeebu et al (1998) and in murine splenocytes exposed to cadmium reported by Pathak and Khandelwal, (2006) also showed that cadmium can potentially induce oxidative stress and programmed cell death (apoptosis). Presence of heavy metals in the leachate samples beyond permissible limits may cause these metals to bio accumulate in the liver, kidney and other organs which may result in cellular or DNA damage or at times induce programmed cell death known as apoptosis.…”

Section: Resultsmentioning

confidence: 95%

Genotoxicity and histopathological assessment of raw and simulated leachates exposed to mice

Iyiola¹,

Adeyemi-Ale²,

Anifowoshe³

et al. 2017

Journal of Applied Sciences and Environmental Management

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Indiscriminate solid waste disposal to the environment without proper treatment poses a serious threat to the public health. This study was carried out to investigate genotoxicity of the raw and simulated leachates samples collected from Amilegbe municipal dump site located in Ilorin metropolis in Nigeria. Some of the physicochemical properties of both raw and simulated leachate samples were determined. Mice were exposed to 1%, 2.5%, 5%, 10% and 25% (raw leachate) and 1%, 5% and 10% concentrations (simulated leachate) respectively for 35 days. Distilled water and colchicine were used for negative and positive control respectively. Two standard genotoxicity tests namely abnormal sperm-head morphology and micronucleus (MN) assays were used to assess possible genotoxicity of the raw and simulated leachates samples. Sperm head morphology assay showed some abnormalities (folded, amorphous, banana shaped, two tails, pin tail among others) and the frequencies of the abnormalities increases was concentrationdependent. Congestion, necrosis, degeneration and appearance of vacuolation were observed in the histopathological analysis of the liver. The histopathological changes were also more pronounced with higher concentrations of raw and simulated leachates. MN and abnormal nuclei frequencies also showed statistically significant differences (p>0.05) such that MN and other nuclear abnormalities reached the maximum at the highest concentration (25% >10% >5% >2.5%>1%). This study shows that the raw and simulated leachates contain potentially genotoxic and cytotoxic substances capable of causing DNA damage. ©JASEM https://dx.doi.org/10.4314/jasem.v21i5.11

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Section: Resultsmentioning

confidence: 95%

Genotoxicity and histopathological assessment of raw and simulated leachates exposed to mice

Iyiola¹,

Adeyemi-Ale²,

Anifowoshe³

et al. 2017

Journal of Applied Sciences and Environmental Management

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“…Cd enhances oxidative burst in cells and affects cellular DNA (Pathak and Khandelwal, 2006b). Thus Cd induces the production of cellular reactive oxygen species (ROS), particularly singlet oxygen, hydroxyl radicals, superoxide radical (…”

Section: J U S T a C C E P T E Dmentioning

confidence: 99%

“…O 2 ) and hydrogen peroxide (Lopez et al, 2006). Tissue increased levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) are the proven indicators of oxidative stress Khandelwal, 2006b, Pathak andKhandelwal, 2006a). However, the induced production of ROS is indirect, as Cd is not a redox-active metal and cannot itself direct the Fenton type of reactions.…”

Section: J U S T a C C E P T E Dmentioning

confidence: 99%

Cadmium induces oxidative stress and apoptosis in lung epithelial cells

Kumar

Patil

et al. 2016

Toxicology Mechanisms and Methods

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Abstract:Cadmium (Cd) is one of the well-known highly toxic environmental and industrial pollutants.Cd first accumulates in the nucleus, and later interacts with zinc finger proteins of antiapoptotic genes; inhibit the binding of transcriptional factors and transcription. However, the role of Cd in oxidative stress and apoptosis is less understood. Hence the present study was undertaken to unveil the mechanism of action. A549 cells were treated with or without Cd

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“…by exposure to a teratogen) has been shown to cause embryonic developmental injury [9,10]. Many of the chemical and physical treatments that induce apoptosis stimulate oxidative stress via generation of ROS (reactive oxygen species) [9,[11][12][13], suggesting a close relationship between oxidative stress and apoptosis. While the precise molecular mechanisms underlying apoptosis…”

Section: Introductionmentioning

confidence: 99%

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

Chan

2007

Biochemical Journal

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The mycotoxin CTN (citrinin), a natural contaminant in foodstuffs and animal feeds, has cytotoxic and genotoxic effects on various mammalian cells. CTN is known to cause cell injury, including apoptosis, but the precise regulatory mechanisms of CTN action, particularly in stem cells and embryos, are currently unclear. In the present paper, I report that CTN has cytotoxic effects on mouse embryonic stem cells and blastocysts, and is associated with defects in their subsequent development, both in vitro and in vivo. Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3. In this model, CTN triggers cell death via inactivation of the HSP90 [a 90 kDa isoform of the HSP (heat-shock protein) family proteins]/multichaperone complex and subsequent degradation of Ras and Raf-1, further inhibiting anti-apoptotic processes, such as the Ras → ERK (extracellular-signal-regulated kinase) signal transduction pathway. In addition, CTN causes early developmental injury in mouse ESCs and blastocysts in vitro. Lastly, using an in vivo mouse model, I show that consumption of drinking water containing 10 µM CTN results in blastocyst apoptosis and early embryonic developmental injury. Collectively, these findings show for the first time that CTN induces ROS and mitochondria-dependent apoptotic processes, inhibits Ras → ERK survival signalling via inactivation of the HSP90/multichaperone complex, and causes developmental injury in vivo.

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Oxidative stress and apoptotic changes in murine splenocytes exposed to cadmium

Cited by 138 publications

References 43 publications

Genotoxicity and histopathological assessment of raw and simulated leachates exposed to mice

Genotoxicity and histopathological assessment of raw and simulated leachates exposed to mice

Cadmium induces oxidative stress and apoptosis in lung epithelial cells

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

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