Metallothionein common inducers

Nutritional status Many antioxidants are present in the diet (e.g., vitamin E, vitamin C, peptides for the synthesis of glutathione, trace metals, and minerals like zinc). However, poor nutrition or malabsorption leads to deficiency of these key vitamins and antioxidants. This may impair the antioxidative defense capacity, leading to drug-induced oxidative stress and lower threshold for DILL In a preclinical study, a mere 1.6- and 2.1-fold increase in liver zinc content was associated with an increase in liver metallothionein between 50- and 200-fold.38 Metallothionein is a key antioxidant protein in vivo capable of scavenging most common kinds of oxidative species.39 It is therefore conceivable that a lack of sufficient dietary available zinc could compromise a patient s hepatic metallothionein levels and his or her antioxidant reserve capabilities in liver. 

SmtB and ArsR have evolved from a common evolutionary origin. They function as a repressor binding to, in the case of SmtB, the smt operator-promoter in the absence of metal ions. On binding Zn(II), the SmtB repressor changes conformation, dissociates from the DNA and induces expression of a metallothionein, a class of cysteine-rich low-molecular-weight proteins. 

The differences in sensitivity to Cd toxicity between phytoplankton species may be related to differences in their ability to detoxify the metal [43,44]. Cd-induced phyto-chelatin production is the most common detoxification mechanism in phytoplankton (see Section 5.1), but other thiol-containing peptides or proteins may also be involved. For example, a Cd-tolerant phytoplankton species, Isochrysis galbana, produces a metal-binding protein rich in cysteine [54] the cyanobacterium Synechococcus sp. produces a metallothionein-like protein to complex metals [55]. In addition, some species may induce efflux systems to remove intracellular Cd [47,56,57], or sequester Cd into the vacuole to reduce the cytosohc Cd concentration [58]. 

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