▁should ▁not ▁be ▁used ▁in ▁the ▁absence ▁of ▁a ▁serious ▁indic ation . ▁ ▁The ▁mechanism ▁of ▁action ▁of ▁fl ut am ide - indu ced ▁he pat ot ox icity ▁is ▁thought ▁to ▁be ▁due ▁to ▁mit och ond rial ▁to x icity . ▁Specifically , ▁fl ut am ide ▁and ▁particularly ▁its ▁major ▁met abol ite ▁hydro xy fl ut am ide ▁in hib it ▁en zym es ▁in ▁the ▁mit och ond rial ▁electron ▁transport ▁chain ▁in ▁he pat ocy tes , ▁including ▁resp ir atory ▁complex es ▁I ▁( N AD H ▁u bi quin one ▁ox id ored uct ase ), ▁II ▁( su cc inate ▁de h ydro gen ase ), ▁and ▁V ▁( AT P ▁synth ase ), ▁and ▁thereby ▁reduce ▁cell ular ▁resp iration ▁via ▁ATP ▁de ple tion ▁and ▁hence ▁decrease ▁cell ▁surv ival . ▁In hib ition ▁of ▁t au ro ch olate ▁( a ▁b ile ▁acid ) ▁eff l ux ▁has ▁also ▁been ▁imp licated ▁in ▁fl ut am ide - indu ced ▁he pat ot ox icity . ▁In ▁contrast ▁to ▁fl ut am ide ▁and ▁hydro xy fl ut am ide , ▁which ▁sever ely ▁comprom ise ▁he pat ocy te ▁cell ular ▁resp iration ▁in ▁vit ro , ▁b ical ut am ide ▁does ▁not ▁significantly ▁do ▁so ▁at ▁the ▁same ▁concentr ations ▁and ▁is ▁regarded ▁as ▁non - mit ot ox ic . ▁It ▁is ▁thought ▁that ▁the ▁nit ro ar om atic ▁group ▁of ▁fl ut