Stressor: 635
Title
Arsenic
Stressor Overview
AOPs Including This Stressor
AOP Name | Evidence |
---|---|
Oxidation and antagonism of reduced glutathione leading to mortality via acute renal failure | Moderate |
Events Including This Stressor
Chemical Table
User term | DTXID | Preferred name | Casrn | jchem_inchi_key | indigo_inchi_key |
---|---|---|---|---|---|
Arsenic | DTXSID4023886 | Arsenic | 7440-38-2 | RQNWIZPPADIBDY-UHFFFAOYSA-N | RQNWIZPPADIBDY-UHFFFAOYSA-N |
AOP Evidence
Oxidation and antagonism of reduced glutathione leading to mortality via acute renal failure
There is no evidence text for this AOP
Event Evidence
Chronic reactive oxygen species
There is no evidence text for this event.
Increases in cellular reactive oxygen species
There is no evidence text for this event.
Inhibition, Mitochondrial Electron Transport Chain Complexes
Prakash, Soni, and Kumar (2015) measured the level of inhibition of mitochondrial electron transport chain complexes in rat brains after exposure to sodium arsenite in their drinking water for 12 weeks. They found that CII (32%), CIV (35%), and CI (42%) were all significantly inhibited (Prakash, Soni, and Kumar, 2015).
Increase, Oxidative Stress
Bhadauria and Flora (2007) studied the effects of arsenic treatment on rat kidneys. They found that lipid peroxidation levels were increased by 1.5 times and the GSH/GSSG ratio was decreased significantly (Bhadauria and Flora, 2007).
Kharroubi et al. (2014) also investigated the effect of arsenic treatment on rat kidneys and found that lipid peroxidation was significantly increased, while GSH content was significantly decreased.
In their study of the effects of arsenic treatment on rat kidneys, Turk et al. (2019) found that lipid peroxidation was significantly increased while GSH and GPx renal content were decreased.
Occurrence, Kidney toxicity
Kharroubi et al. (2014) investigated the histological effects of arsenate on rat kidneys. In their study, they found that the arsenate-treated groups had glomerular atrophy and showed an expansion of the area between the glomeruli and the Bowman’s capsule, indicating that renal corpuscular degeneration was occurring (Kharroubi et al., 2014). When Kharroubi et al. (2014) examined renal functional markers in response to two different doses and two different time periods of arsenate, they found a dose- and time-dependant increase in serum creatinine and urea, and a decrease in total protein (Kharroubi et al., 2014).
In their study of the effects of arsenite treatment on rats, Turk et al. (2019) found that the arsenic treated group showed much more necrosis than the control, including hydropic degeneration in the tubulus epithelia, dilation in the Bowman’s capsule, and coagulation necrosis. They also noted increased IL-6 content in the kidney tissues of the treated rats, indicating that inflammation was occurring. Turk et al. (2019) also found that serum urea and serum creatinine in the arsenic-treated group were significantly increased compared to the control levels.
Oxidative Stress
Bhadauria and Flora (2007) studied the effects of arsenic treatment on rat kidneys. They found that lipid peroxidation levels were increased by 1.5 times and the GSH/GSSG ratio was decreased significantly (Bhadauria and Flora, 2007).
Kharroubi et al. (2014) also investigated the effect of arsenic treatment on rat kidneys and found that lipid peroxidation was significantly increased, while GSH content was significantly decreased.
In their study of the effects of arsenic treatment on rat kidneys, Turk et al. (2019) found that lipid peroxidation was significantly increased while GSH and GPx renal content were decreased.
Increase, Cytotoxicity (renal tubular cell)
Turk et al. (2019) treated rats with arsenic and observed the kidneys for biochemical changes. Their results showed increased caspase-3 activity in the treated kidneys, indicating an increase in cellular death when the cells were treated with arsenic (Turk et al., 2019).