Collectively, our results indicate that GCM alleviated acetaminophen-induced oxidative stress through activating autophagy, thereby protecting against AILI. Our findings suggest that GCM has potential as a novel therapeutic agent for treating AILI.
Previous
studies have shown that selenite, a representative of
inorganic form selenium, exerts its anticancer effect by inducing
apoptosis in androgen-dependent LNCaP prostate cancer cells, but few
studies have determined the nature of cell death induced by selenite
in metastatic androgen-refractory PC-3 cells. Our study showed that
necrosis-like cell death rather than apoptosis, pyroptosis, or autophagic
cell death was caused by selenite in PC-3 cells. Mechanistically,
this type of cell death was caused by ATP depletion (26.28 ±
3.39 nmol/mg of control versus 9.12 ± 2.44 nmol/mg of 10 μM
selenite treatment) that resulted from phosphofructokinase activity
reduction (100.17 ± 0.17% of control versus 21.74 ± 6.65%
of 10 μM selenite treatment). Our study also showed that ROS
production is necessary for the decrease in cellular ATP levels and
in phosphofructokinase activity. To our knowledge, this is the first
study showing that selenite can induce necrosis-like cell death in
PC-3 cells. Our findings support selenite as an effective compound
for the therapy of apoptosis-resistant prostate cancer.
Patulin (PAT) is the most common food-borne mycotoxin found in fruits and fruit-derived products, while chlorpyrifos (CPF) is a widely used pesticide on fruit and other crops. On the basis of the residue data, certain types of fruits can be contaminated simultaneously by patulin and chlorpyrifos. However, there are no available data about the combined toxicity. Since liver is a possible toxic target of both patulin and chlorpyrifos, we tested whether the combination exposure can cause enhanced hepatotoxicity using both cell culture and animal models. Results showed that the combination resulted in synergistic cytotoxicity in vitro and significantly enhanced liver toxicity in vivo. Mechanistically, PAT inhibited catalase activity via PIG3 induction, while CPF decreased catalase expression. These two mechanisms were converged in response to the combination, leading to enhanced inactivating catalase and boosted reactive oxygen species generation. The finding implicated that it is necessary to consider the combined toxicity in safety assessment of these food-borne contaminants.
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