UGT B is involved in the glucuronidation of catechol

UGT2B7 is involved in the glucuronidation of catechol estrogens, bile acids, morphine, MPA, oxazepam and zidovudine with overlapping substrate specificities (Mackenzie et al., 2003). Additionally, UGT2B7∗2 allele is affiliated with defective morphine glucuronidation in vitro and hence, homozygous infants with the UGT2B7∗2 allele, may be at an enhanced risk of potential life-threatening CNS depression after codeine treatment (Coffman et al., 1997; Ishii et al., 1997). In fact, UGT2B7 exclusively catalyzes the glucuronidation of codeine, morphine and zidovudine (AZT) (Barbier et al., 2000) and non-drug xenobiotic substrates including hydroxylated derivatives of the prototypic carcinogens 2-acetylaminofluorene and benzo[a]-pyrene. Despite being primarily involved in the detoxification of xenobiotic and endogenous substrates, UGT2B7 also plays a vital role in forming bioactive or even toxic compounds like the highly cholestatic D-ring glucuronides of estrogens and the acyl-glucuronides of drugs such as diflunisal that binds to proteins and triggers toxic immunological responses (Worrall and Dickinson, 1995). Various studies have demonstrated that UGT2B7∗2 polymorphism nominally impacts enzyme activity and substrate specificity of UGT2B7 (Coffman et al., 1998; Holthe et al., 2002a,b; Bhasker et al., 2000). However, a wide inter-individual variance in the ability to glucuronidate morphine (McQuay et al., 1990; Klepstad et al., 2000; Faura et al., 1998) and AZT (Mentre et al., 1993) suggests that this or other polymorphisms in UGT2B7 may contribute to morphine metabolism variability.
UGT2B15∗2 glucuronidates many drugs such as oxazepam, lorazepam and rofecoxib. Our data indicate that heterozygous repeat of UGT2B15∗2 accounts for about 62% of the study population. Studies have shown that prostate cancer patients are significantly more likely to be homozygous for the lower activity UGT2B15∗2 allele than control individuals (Holthe et al., 2000a,b) Homozygous repeat glucose assay represent increased risk of prostate cancer associated with this low activity variant. Therefore, our data indicate that Saudis are at a low risk of being afflicted with prostate cancer.

Conclusion

Acknowledgments
This study was supported by the National Plan For Science and Technology Program (NPST)-King Saud University (Grant 08-MED565-02), King Abdulaziz City for Science and Technology, Riyadh, Saudi Arabia.

Introduction
The increase of reactive oxygen species (ROS, known as free radicals) levels in living organisms, as a result of metabolism, environmental exposure and aging, can ultimately contribute to cell death induced by several harmful events on cell structures, such as DNA, RNA, proteins and lipids (Hosain et al., 2016; Nakazawa et al., 2016). The use of anti-oxidants to protect cells from excess of ROS and to delay the cells aging and death is, therefore, a regular practice.
Tocopherols are a family of natural and synthetic compounds, being d-α-tocopherol or vitamin E the most popular member, and are preferentially absorbed and accumulated in humans (Brigelius-Flohé and Traber, 1999). These molecules contain two main structural elements, the chromanol head (benzodihydropyran containing an alcohol group), and the phytyl tail consisting of repeats of saturated isoprenoid units. d-α-tocopherol has antioxidant function, by scavenging peroxyl radicals, and is able to protect the lipids, present in the fat phase of foodstuff, as well as those in membrane of living cells, from auto-oxidation (Atkinson and Traber, 2007). However, like other lipophilic compounds, d-α-tocopherol is poorly soluble in water and is highly sensitive to various environmental factors, such as light, oxygen, alkali and temperature (Zigoneanu et al., 2008).
In order to improve its biological stability during manufacturing and storage, d-α-tocopherol has been incorporated in nanocarriers. Several studies report the use of different types of nanocarriers to promote the antioxidant activity in foodstuff, as well as to preserve its nutritional value. Examples are liposomes (Khanniri et al., 2016), solid lipid nanoparticles and nanostructured lipid carriers (Hentschel et al., 2008; Souto et al., 2005), and micro/nanoemulsions (Kumar et al., 2016; Zheng et al., 2016).