Page 171 - Plant-Based Remediation Processes

162 X.-Z. Yu and J.-D. Gu

9.2.1 Selenium Essentiality

Selenium can be either beneficial or toxic to living organisms, highly depending on
its chemical forms and the dose as well as other environmental regulating variables
(Shardendu et al. 2003). The nutritional benefit of Se for preventing hepatic
necrosis caused by vitamin E deficiency has been reported (Schwarz and Foltz
1957). Se is an essential constituent of the enzyme glutathione peroxidase (GSH-
Px), which is an essential antioxidative system (Rotruck et al. 1973). GSH-Px
assists in intracellular defense mechanisms against oxidative damage by preventing
and reducing the production of reactive oxygen species (ROS) (Ursini and Bindoli
1987). More than 10 Se-containing proteins have been identified/or isolated,
indicating that Se is not merely restricted to its role in antioxidant activity but
also involved in other multiple aspects of mammalian metabolism (Tinggi 2003).
The most famous case associated with Se deficiency is Keshan disease occurred in
young Chinese children and women of childbearing age living in the low Se-belt
regions in China (Wang and Gao 2001). It has been proposed that Se deficiencies in
animals can be observed when diets contain less than 0.05–0.10 mg Se kg 1 (Milne
1998), or blood Se concentration is below 0.05 μgL 1 usually associated with
clinical disease for people (Mass 1998). In spite of its nutrition and benefit to
animals and humans, the question on the essentiality of Se as a micronutrient in
higher plants is unresolved and remains controversial (Terry et al. 2000).

9.2.2 Mechanisms of Selenium Toxicity

Selenium supplementation with nutrient levels is able to increase GSH-Px
activities, which is responsible for scavenging free radicals and neutralizing their
potential damage (Hartikainen et al. 2000). However, oversupply of Se above the
threshold of nutrition limit, in turn, increases oxidative stress and contributes to the
formation of ROS (Seko and Imura 1997). ROS are generated as intermediates of a
number of metabolic reactions in cellular organelles of different living organisms
(Kitahara et al. 1993; Spallholz 1994). Inorganic Se compounds stimulate the
formation of ROS, either by direct electron transfer involving cationic metals or
as a consequence of metal-mediated inhibition of metabolic reactions (Halliwell
and Gutteridge 1999). ROS can result in the damage of DNA, proteins, and
pigments as well as initiating lipid peroxidation (Panda and Khan 2003). Adequate
defense against oxygen toxicity requires efficient scavenging of ROS, e.g., super-
oxide radicals and hydrogen peroxide (Tsang et al. 1991). Superoxide radicals are
toxic by-products of oxidative metabolism (Fridovich 1978). Toxicity of superox-
ide radicals has been attributed to its interaction with hydrogen peroxide to form
highly reactive hydroxyl radicals, which are thought to be largely responsible for
mediating oxygen toxicity in vivo (Fridovich 1978). The toxicity of Se at higher
concentrations is thought to be mainly due to its chemical similarity to sulfur (S),