Zinc intoxication may cause anemia by blocking the absorption of copper from the stomach and duodenum .  Zinc also upregulates the expression of chelator metallothionein in enterocytes , which are the majority of cells in the intestinal epithelium.  Since copper has a higher affinity for metallothionein than zinc, the copper will remain bound inside the enterocyte, which will be later eliminated through the lumen .  This mechanism is exploited therapeutically to achieve negative balance in Wilson’s disease , which involves an excess of copper. 
The most frequent adverse reactions to Efudex occur locally and are often related to an extension of the pharmacological activity of the drug. These include burning, crusting, allergic contact dermatitis , pruritus , scarring, rash, soreness, and ulceration . Ulcerations, other local reactions, cases of miscarriage and a birth defect ( ventricular septal defect ) have been reported when Efudex was applied to mucous membrane areas. Leukocytosis is the most frequent hematological side effect. Although a causal relationship is remote, other adverse reactions which have been reported infrequently are:
Riluzole is administered orally. Riluzole is highly bound to plasma protein (about 96%), mainly to albumin and lipoproteins. Hepatic metabolism is extensive, producing 6 major and a number of minor metabolites. The cytochrome P450 enzyme system is involved in hydroxylation and glucuronidation. The main isozyme involved in hydroxylation is CYP1A2. Approximately 90% of a dose is excreted in the urine; however, only 2% is excreted as unchanged drug. Elimination in the feces accounts for 5% of a dose. Riluzole is largely excreted as its glucuronide metabolites (85%). The elimination half-life is 12 hours.
Affected cytochrome P450 isoenzymes and drug transporters: CYP1A2
Riluzole is primarily metabolized by CYP1A2.