# A Review on Potential Antimutagenic Plants of Saudi Arabia
## 5 What Are the Strategies for Minimizing Mutagenic Complications?  
One of the approaches to preventing mutation-related complications is to avoid exposure to mutagens or to increase the intake of substances that possess antimutagenic properties. Since oxidative stress is the chief reason for mutation, compounds having the ability to increase antioxidant status are reported to exhibit anti-mutagenic potential [45]. These substances are known to balance the outcome of ROS through enzymatic and non-enzymatic pathways. The substances provide excellent defences as they directly remove free radicals from the biological system [46].  
The literature suggests that methods by which the anti-mutagens wield their effects are complex and often involve multiple activities. The important activities reported for dietary and endogenous antioxidants include pharmacokinetic alterations in absorption, protein binding, metabolism (detoxification), activation of mutagens and DNA repair processes [47]. Interference with the P450-dependent biotransformation of mutagens is one of the most specific mechanisms by which dietary components exert their effects [48].  
Some of the known antioxidants, such as vitamins, have been reported to reduce DNA damage. Their action involves breaking down a chain of events essential for mutagenesis and can contribute to DNA repair mechanisms [30]. According to literature, one of the main damaging intracellular ROS is hydroxyl radical (\(\bullet\)OH) and vitamin E has reduced H\({}_{2}\)O\({}_{2}\)-induced \(\bullet\)OH production and successive DNA base pair adjustment in host cells. Vitamin E is also reported to provide an inhibitory effect against the peroxuritirite mediated DNA damage that is produced by immune cells during inflammation [49].  
In addition to this, Vitamin E administration during radiation therapy to bone marrow polychromatic erythrocytes, reduced oxidative stress-induced micronucle development. These inhibitory effects were reportedly due to the antioxidant potential as well as the modulation of DNA repair structures and exclusion of damaged DNA from host cells [50]. In another study, it was observed that Vitamin A or retinol exhibited antimutagenic activity due to its antioxidant properties. It was found to attenuate the oxidative stress-induced DNA defects produced by benzo (a) pyrene, cyclophosphamide, aflatoxin B and 3-methyl cholanthrene. Furthermore, the anti-mutagenic effects of vitamin A were also reported against N-nitroosamine compounds, quinoline derivatives, methyl methane sulfonate (MMS) and bovine papilloma virus. The methods used to identify the anti-mutagenic property were DNA fragments, sister-chromatid exchanges, micronuclele frequency and chromosomal aberrations in different types of rodent cells [51]. Retinol, a known dietary antioxidant, exhibited these effects by scavenging the chemical mutagens and their metabolites. In addition, other mechanisms suggested for anti-mutagenic activity include DNArepair, prevention of conversion of oncogenic metabolites, and enhanced elimination of chemical mutagens [52]. Further, the deficiency of vitamin A in some patients has been associated with higher incidences of breast cancer [53].  
The research conducted on vitamin C/ascorbic acid suggests that it possesses antioxidant properties against a variety of free radicals such as ONOO-, NO2, NO and hypochlorous acid. Vitamin C has been tested extensively against mutagenic difficulties induced by oxidative stress and was shown to mitigate the changes induced by gamma-irradiation [54]. In addition, vitamin C supplementation was found to rejuvenate other antioxidants such as glutathione and caroten. The ability of vitamin C to prevent mutagenic complications has been linked to reduced chances of carcinogenesis [55].