Pearls, Pitfalls, and Updates in Toxicology

Kirk, Mark A.; Pace, Steven

doi:10.1016/s0733-8627(05)70309-6

Cited by 14 publications

(3 citation statements)

References 87 publications

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“…A role for NAC as an anti-dote for poisoning has already been reported [21]. Hence, the observation that certain bacterial toxins acting as enteropathogenic virulence factors provoke oxidative stress in cells is a new point of view which may provide some clues to the pharmacological control of their intoxication-associated cytopathology.…”

Section: Discussionmentioning

confidence: 96%

“…In conclusion, taken together, all the above reported results clearly indicate that C. difficile toxins cause oxidative imbalance in epithelial cells which can be counteracted by anti‐oxidant compounds acting as thiol suppliers, such as NAC. A role for NAC as an anti‐dote for poisoning has already been reported [21]. Hence, the observation that certain bacterial toxins acting as enteropathogenic virulence factors provoke oxidative stress in cells is a new point of view which may provide some clues to the pharmacological control of their intoxication‐associated cytopathology.…”

Section: Discussionmentioning

confidence: 96%

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N‐Acetylcysteine protects epithelial cells against the oxidative imbalance due to Clostridium difficile toxins

et al. 1999

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Toxins A and B from the anaerobic bacterium Clostridium difficile are the causative agents of the antibioticassociated pseudomembraneous colitis. At the subcellular level, they inhibit the Rho family GTPases, thus causing alterations of the actin cytoskeleton. The cytoskeletal integrity is also controlled by the redox state of cells. Therefore, we have evaluated whether an oxidative imbalance could be involved in the toxin-induced cytopathic effects. Our results indicate that both toxins induce oxidative stress with a significant depletion of protein SH-groups. These responses and the cytoskeletondependent cell retraction and rounding are significantly counteracted by N-acetylcysteine but not by K K-tocopherol. Our study provides the first evidence that the thiol supplier N-acetylcysteine impairs the cellular intoxication by acting on the cytoskeleton integrity. This also suggests a possible beneficial role for this drug during therapeutic intervention.z 1999 Federation of European Biochemical Societies.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

N‐Acetylcysteine protects epithelial cells against the oxidative imbalance due to Clostridium difficile toxins

et al. 1999

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“…NAC is used in the therapy of many diseases, e.g. acute pancreatitis [14], chronic obstructive bronchitis [4], chronic renal diseases [11], in some acute poisonings [7]. However, the mechanisms underlying the effects of ROS and antioxidants (including NAC) remain unclear.…”

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confidence: 99%

Decreased sensitivity of transformed 3T3-SV40 cells treated with N-acetylcysteine to bacterial invasion

et al. 2006

Bull Exp Biol Med

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Long-term treatment of transformed 3T3-SV40 mouse fibroblasts with antioxidant N-acetylcysteine decreased cell level of ROS and increased the concentration of reduced glutathione. Removal of N-acetylcysteine from the medium led to the appearance of well-expressed stress fibrils, virtually absent in control cells. In contrast to control cells, these cells were not invaded by apathogenic Escherichia coli A2 strain producing ECP32 protease specifically cleaving actin. Antioxidant N-acetylcysteine can cause partial reversion of transformed phenotype at the expense of a shift of cell redox balance in favor of reduced glutathione.

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Barbiturates

Walsh¹,

Katz²

2017

Critical Care Toxicology

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Pearls, Pitfalls, and Updates in Toxicology

Cited by 14 publications

References 87 publications

N‐Acetylcysteine protects epithelial cells against the oxidative imbalance due to Clostridium difficile toxins

N‐Acetylcysteine protects epithelial cells against the oxidative imbalance due to Clostridium difficile toxins

Decreased sensitivity of transformed 3T3-SV40 cells treated with N-acetylcysteine to bacterial invasion

Barbiturates

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