 N @-@ Acetylcysteine has shown promise in combination with other therapies . Animal studies indicate the amatoxins deplete hepatic glutathione ; N @-@ acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage . None of the antidotes used have undergone prospective , randomized clinical trials , and only anecdotal support is available . Silibinin and N @-@ acetylcysteine appear to be the therapies with the most potential benefit . Repeated doses of activated carbon may be helpful by absorbing any toxins returned to the gastrointestinal tract following enterohepatic circulation . Other methods of enhancing the elimination of the toxins have been trialed ; techniques such as hemodialysis , hemoperfusion , plasmapheresis , and peritoneal dialysis have occasionally yielded success , but overall do not appear to improve outcome . 
