Saturday, March 26, 2011
Shrimp + Vitamin C = arsenic poisoning??
I recently got an email that said a girl in Taiwan suddenly died one night and it was because she ate shrimp and vitamin C together. In the email, it said that later, a professor examined the dead's body and was said it was arsenic poisoning. One day after my family and I ate a large helping of shrimp, I looked on the computer. I found out that that was a total lie! This legend has been going on since 2001! There was many forward emails about this. Check out http://www.truthorfiction.com/rumors/v/vitaminshrimp.htm to see about this fiction rumor.
Subscribe to:
Post Comments (Atom)
Shrimp, Vitamin C & Arsenic poisoning
ReplyDeleteMarine organisms normally contain arsenic residues ranging from < 1 to more than 100 mg/kg, predominantly as organic arsenic species such as arsenosugars (macroalgae) and arsenobetaine (invertebrates and fish). Bioaccumulation of organic arsenic compounds, after their biogenesis from inorganic forms, occurs in aquatic organisms. Bioconcentration factors in freshwater invertebrates and fish for arsenic compounds are lower than for marine organisms. Biomagnification in aquatic food chains has not been observed. Background arsenic concentrations in freshwater and terrestrial biota are usually less than 1 mg/kg (fresh weight).
With the exception of fish, most foods contain less than 0.25 µg/g arsenic. Many species of fish contain between 1 and 10 µg/g. Arsenic levels at or above 100 µg/g have been found in bottom feeders and shellfish. Both lipid- and water-soluble organoarsenic compounds have been found but the water-soluble forms constitute the larger portion of the total arsenic content. The nature of these compounds has been shown to be mainly of the quaternary arsonium type. As was mentioned above, arsenobetaine is believed to be the most predominant species, but recent Canadian results demonstrated a higher level of arsenocholine than arsenobetaine in shrimps.
Vitamin C or L-ascorbic acid or L-ascorbate is an essential nutrient for humans and certain other animal species. In living organisms ascorbate acts as an antioxidant by protecting the body against oxidative stress. It is also a cofactor in at least eight enzymatic reactions including several collagen synthesis reactions that, when dysfunctional, cause the most severe symptoms of scurvy. In animals these reactions are especially important in wound-healing and in preventing bleeding from capillaries.
Ascorbate (an ion of ascorbic acid) is required for a range of essential metabolic reactions in all animals and plants. It is made internally by almost all organisms although notable mammalian group exceptions are most or all of the order chiroptera (bats), guinea pigs, capybaras, and one of the two major primate suborders, the Anthropoidea (Haplorrhini) (tarsiers, monkeys and apes, including human beings). Ascorbic acid is also not synthesized by some species of birds and fish. All species that do not synthesize ascorbate require it in the diet. Deficiency in this vitamin causes the disease scurvy in humans. It is also widely used as a food additive.
Although there is no compelling evidence that vitamin C has antitumor activity in humans, clinical trials are testing the hypothesis that ascorbic acid will enhance the efficacy of arsenic trioxide (As2O3) in myeloma. In vitro, ascorbic acid cytotoxicity depends on its interaction with free transition metal ions in culture media leading to the generation of H2O2 and other reactive oxygen species. To circumvent the extracellular in vitro pro-oxidant effects of ascorbic acid, HL60, U266, and RPMI-8226 cells are loaded with vitamin C by incubation with dehydroascorbic acid. Loading cells in this manner resulted in prominent, dose-dependent protection of As2O3-treated cells as measured by viability, colony formation, and apoptosis assays. Glutathione depletion enhanced cell sensitivity to the cytotoxic effects of As2O3 and vitamin C loading provided protection. Ascorbic acid was found to generate cytotoxic concentrations of H2O2 in culture medium without cells and copper/iron chelators inhibited this reaction. However, ascorbic acid did not generate H2O2 in simple buffer or human plasma. Direct incubation with ascorbic acid resulted in increased intracellular reactive oxygen species , whereas dehydroascorbic acid incubation decreased it. These results clarify an apparent paradox and indicate that vitamin C loading in HL60, U266, and RPMI-8226 cells ameliorates As2O3 cytotoxicity.
Nalliah Thayabharan