Freddd said : Glutathione combines chemically with the cobalamin, doesn't matter which one in this case. It's like cyanide. It combines with it. For whatever the reason once the glutathione combines with what appears to be about 100% of the unbound b12 in the body and flushes it out through the urine, very visiably if a person has any significant amount. The molecular mass of MeCbl is about 1350 (several variations). The CH4 stripped off is 1.3% of the mass , so the rest of the cobalamin is attached to glutathione making glutathionyl cobalamin. If a person takes causes 1000mg of glutathione to be made that could destroy 5000mg or more of MeCbl. Since a person has typically 1mg to 100mg in somebody using a lot, there is vasrt overkill of glutathione regardless of the exact amounts. When this b12 is swept from the body the person goes onto methyltrap, in 2-3 hours if the dose of glutathione is large enough. Now if the person is already in methyltrap, they don't notice a thing except perhaps some relief from neurological pain and whatever else the glutathione is doing. Glutathione, when I was taking 30mg a day, had a coloration equal to 60mg in the toilet bowl. The only thing comparable was taking multi hundred mg doses by injection as far as the coloration goes. The difference was that in that N=10 trial, was that everybody tjhat tried the glutathione was already sucessfully healing and was out of methyl block. Every one of us went back into methylblock in hours to a day (whey was way slower). You can experiment for yourself. First tun on healing. Start feeling pretty good for some months and then try glutathione and you will feel yourself being cast back into the pits of hell as symptoms return and getting worse by the day. In six weeks a person can go from health to very sick. If you use glutathione during methyltrap it will only make it worse but the person can't feel it. I found the arguments strong enough to convinve me to try it with 9 other people. I was very hopeful it would work. I was looking what would fix me and others. The omne thing I can tell you for sure. The people taking glutathione do not get well as long as they are taking it. They may quibble about how they feel. They do not largely heal in year. Healing does not turn on while they are taking it. As some others found out who had never had healing turn on when they discontinued the glutathione already being taken at the same time as MeCbl etc they didn't heal until some while after stopping glutathione and taking the reversal doses.
Rich Vank said : The question of whether to supplement glutathione in some way in conjuction with treatment of the partial methylation cycle block in ME/CFS often comes up. There is some recent research that appears to shed some light on this issue, so I would like to review the status of at least my understanding of it. As I see it currently, there are three groups of people with respect to their response to adding glutathione to methylation treatment: 1. There is a group who benefit from this addition, in terms of their symptomatic response. 2. There is a group who benefit initially, but as time goes on, it causes their symptoms to worsen. 3. There is a group who experience immediate worsening of their symptoms. I dont know what fraction of the ME/CFS population is in each group. I would like to suggest what I think is going on in each of these groups. I suggest that the first group have inherited normal genotypes of their intracellular B12 processing enzymes, and they also have normal status of vitamins B2 and B3. In this group, the glutathione can be recycled at a normal rate when it becomes oxidized by reactive oxygen species that are part of the oxidative stress in ME/CFS, by the glutathione reductase reaction, which requires both B2 and B3. Furthermore, glutathione is able to play its normal roles with respect to the intracellular processing of vitamin B12. In particular, the Cblc enzyme (also known as MMACHC) uses glutathione to remove the upper ligand from incoming forms of B12 (cyano-, methyl- or adenosyl-) by the formation of glutathione conjugates of these ligands (PMID: 19801555). In addition, it appears that glutathione also reacts with the resulting aquocobalamin to form glutathionylcobalamin. Glutathionylcobalamin is chemically more stable than the other forms of B12, but Cbcl is normally able to retrieve cobalamin from glutathionylcobalamin so that the cobalamin can be used to form methylcobalamin and adenosylcobalamin in the amounts needed by the cell (PMID: 21429294). Thus, glutathione appears to serve not only as a reactant in the metabolism of B12, but also as a protector of B12 from reactions with toxins, and a buffer to store B12 until it is needed by the cell. I suggest that the second group have inherited normal genotypes of their intracellular B12 processing enzymes, but they have a deficiency in B2 or B3 or both, so that the rate of the glutathione reductase reaction is too slow to keep up with the oxidation of the glutathione. As a result, though the supplemented glutathione is initially beneficial to them, over time it becomes a detriment, because the ratio of reduced to oxidized glutathione drops too low, and this worsens the oxidative stress of the cells. I suggest that the third group has inherited an inborn error of metabolism involving the Cblc enzyme. As a result of this, when glutathione reacts with B12 to form glutathionylcobalamin, their genotype of the Cblc enzyme is unable to retrieve the cobalamin from the glutathione to use it to form methylcobalamin and adenosylcobalamin. If glutathione is supplemented, this situation is made worse for this group. In addition, this group is unable to make use of hydroxocobalamin as their B12 supplement (PMID: 21497120), because it is converted to glutathionylcobalamin in their cells (even without supplementing glutathione) and is therefore made inaccessible. I suggest that Freddd is in this group, and this explains why he cannot tolerate supplementing glutathione, why he cannot make use of cyanocobalamin or hydroxocobalamin, and why he must use high dosages of methylcobalamin and adenosylcobalamin, applied either sublingually or by injection. This raises the concentration of these species in the blood stream, and enough of them is able to diffuse into the cells through their plasma membranes to be used directly without intracellular processing, thus supplying the need of his cells for methylcobalamin and adenosylcobalamin.
Freddd said : The one thing I will be clear about is that aside from ignoring hypokalemia and calling it detox, the most potentially damaging thing a person can do is take glutathione above a certain unknown level and keep taking it. In 6 weeks it can cause or worsen brain and cord damage in Subacute combined degeneration and it's first cousin, MS is also likely rapidly increased damage. It can cause high MCV and high MCH and half a dozen other blood changes on the first 3 months (the problems happen right away but blood cells stick around 3-4 months so it takes a while ot see). Doing a risk assessment of this is probably a good idea. A researcher I have spoken with who has approiached these matters from a different direction told me, in person and on the phone, that "There is probably no safe way to take glutathione." The subjective benefits I too have felt. When there is neurological pain, it reduces the neurological pain by damaoing the nerves to numbness so even perveived benefit is dangerous and damaging. That can be perceived in the first days, as I perveived it, before the effects of methyltrap become felt. Those who are not in methyltrap and are doing welll will be the ones who will feel the worst onset of glutathione.
Rich Said : I suggest that the third group has inherited an inborn error of metabolism involving the Cblc enzyme. As a result of this, when glutathione reacts with B12 to form glutathionylcobalamin, their genotype of the Cblc enzyme is unable to retrieve the cobalamin from the glutathione to use it to form methylcobalamin and adenosylcobalamin. If glutathione is supplemented, this situation is made worse for this group.
Since Rich is basing this hypothesis on me, based on old incorrect hypothses concerning my own supposed inborn error in the CblC enzyme whic isabsolutely 100% wrong for me and all of the N=10 group, all logic flowing from this assumption is 100% wrong.
In addition, this group is unable to make use of hydroxocobalamin as their B12 supplement.
This assumption is also 100% wrong concerning the people in the N=10 group trial. Some of those were vegetarians. One man had such amazingly good response to HyCbl that it got him out of a wheelchair but the HyCbl could take it no further. He needed MeCbl and AdoCbl to get rid of the walker frame and return to work.
because it is converted to glutathionylcobalamin in their cells (even without supplementing glutathione) and is therefore made inaccessible. I suggest that Freddd is in this group, and this explains why he cannot tolerate supplementing glutathione, why he cannot make use of cyanocobalamin or hydroxocobalamin, and why he must use high dosages of methylcobalamin and adenosylcobalamin, applied either sublingually or by injection. This raises the concentration of these species in the blood stream, and enough of them is able to diffuse into the cells through their plasma membranes to be used directly without intracellular processing, thus supplying the need of his cells for methylcobalamin and adenosylcobalamin.
Again, all of this is based on assumptions that are 100% WRONG!
it appears that glutathione also reacts with the resulting aquocobalamin to form glutathionylcobalamin. Glutathionylcobalamin is chemically more stable than the other forms of B12, but Cbcl is normally able to retrieve cobalamin from glutathionylcobalamin so that the cobalamin can be used to form methylcobalamin and adenosylcobalamin in the amounts needed by the cell (PMID: 21429294).
While this may be sort of correct in terms of normal amounts of glutathione, in these much larger doses beiong taken, this is NOT CORRECT. The glutathione combined dirrectly with AdoCbl and MeCbl that is in serum or cells and changes there again and again faster than the body can convert it back to usable forms, This is demonstrable. No amount of injected MeCbl taken with large amounts of glutathione survive to be used. The whole thing is based on a first approximation understanding that upon more iuderstanding has been proven totally wrong. Rich was unwilling to reconsider my situation because it fit his theories so nicely. As everything he thinks about my biochemistry as regards B12 and folates is wrong, all of his suggestions and conclusions based on that are wrong. This entire statement is too badly flawed to be any valid usage and anybody basing what they do on it is at risk of doing unintentional damage to themselves. That entire statement is so flawed that I'm not sure any of it is salvagable.
I would like it much better if somebody knowledgeable could write an understanding of it that isn't based on me as an example and my presumed genetic characteristics and ignore entirely the other 9 in the trial. I have been extremely specific about those who tried it and found the reversal. FIRST they had to have effectiveness of the Active B12 protocol. So whatever argument made can't be about a specific set of rare genes because the people in the N=10 are quite varied, including a vegetarian, using every form. That every form of precursors were approximately as effective as glutathione IV, including NAC alone in some people, shows that it isn't difficult at all to get glutathione into the body. Any explanation has to able to include the actual pragmatic examples within a suitable hypothesis. You can't throw out every bit of contrary information and form the hypothesis on wrong statements and misunderstandings. The above fails that test. When all the logic on who it happens to disappears and even reverses from his statements, there is nothing valid there. It may be possible to form a valid hypothesis from all this that supports glutatathion at certain minimal doses for a short time in people who haven't achieved methylation startup and who are still in methyltrap and not yet achieved ATP startup. If Rich had been willing to discuss this matter and revise his opinions about what is wrong with me based on all the folate information he got me started on, this is what I would have tried to work out with him. As he came to believe that glutathione shouldn't generally be given in any case, he was likely near to be willing to discuss. It was perhaps my disappearing for some months that prevented that. You may not understand how we were interacting. We exchanged information and data. He brought to my attention a variety of flaws, all of which I corrected. I brought flaws to his attention. SOme he considered and made alterations. Some he ignored 100% despite repeated explanation. His hypothesis appeared far more important to him than mine is to me. For me what is important how to solve the probelm, not the specific details of the solution. In order to get good answers one must ask good questions. If there isn't some ancient wisdom to that effect there should be. In the computer age it has been summerized GIGO; Garbage In Garbage Out. That is logic based on flawed assumptions and incorrect data doesn't yield valid results except by accident. In computers if you do everything that wrong the program doesn't run or gives lots of interesting and weird errors. I'm playing "you bet your life" in this 100%. My life is literally at stake in all this, as is yours. Rich was playing science. He was a disinteresrted observer except for protecting his theoretical turf. His life wasn't at stake. His theory was. "Old scientists never die, they just loose track of their data". You know, "Old gymnasts never die, they just can't remount in 30 seconds." I ask questions nobody else who hasn't lived through it can ask. I have possible answers that require experienceto have . In the end a valid hypothesis can explain you and me and Dan and Dbkita et al and have each of us described accurately and predictably. There is a lot to account for, not a lot to throw out or ignore.
As far as understanding MeCbl better: http://health101.org/art_methylcobalamin.htm and it has footnotes. It was written before l-methylfolate and has some things that could be changed. A sample paragraph.
The coenzyme form of vitamin B12 is known as methylcobalamin or methyl B12.It's the only form of vitamin B12 which can directly participate in homocysteine metabolism.In addition, converting homocysteine to methionine via methyl B12 generates an increased supply of SAMe (S-adenosyl methionine), the body's most important methyl donor.Indeed, some of the benefits of methyl B12, such as protection from neurotoxicity, appear to derive from increased production of SAMe8, 9.Methyl B12 has also been reported to be neurotrophic or growth-promoting for nerve cells10, 11, a property which may help regenerate central and peripheral nervous tissues damaged in disorders such as amyotrophic lateral sclerosis12 and diabetic peripheral neuropathy13.
There is no simple right and wrong. Both make valid points. There is increasing medical evidence that aluminium contributes to brain damage. What Dr David Gorski disagrees with, is whether the aluminium in vaccines is a significant source of aluminium toxicity (since some argue that aluminium exposure from foods and environment, is even worse than from vaccines), and therefore whether the risks of vaccinations outweigh the rewards.
Potassium metal cannot be effectively obtained from the electrolysis of molten salts such as potassium chloride. Why? Accordingly, suggest an alternative setup to successfully obtain potassium metal.
Full Question here : http://www.bedokfunlandjc.com/#Qns
During the extraction of sodium metal via electrolysis, often a molten mixture of sodium chloride and calcium chloride is used, instead of pure sodium chloride. Suggest why, and what problems would occur if pure sodium chloride was used instead.
Full Question here : http://www.bedokfunlandjc.com/#Qns
Originally posted by tk2018:
I always find these "So what do you do? What is your background?" kind of questions like some kind of d*ck-measuring contest or pissing match. Pardon the vulgarities (definitely not directed at you), and don't mind me, those are just the first thoughts that come into my mind when I see them :). Especially in the Singapore context. It seems hard to be a "Good Will Hunting" kind of chap to come in and solve difficult academic problems.
Well, since this is the internet (i.e. we can be anyone we say we are), I taught undergraduate chemistry modules in the mecca of science that is by the banks of Charles River, and a hippie town known for drunken revelry and rioting in CA, so hopefully that qualifies me to post suggested answers on this forum! I stumbled into this forum because it's rare to see a Singapore homework forum with high-school/A-level chemistry questions that matched the difficulty of some of my sophomore level classes. Kudos to you!
I still find my A level Chemistry (especially the old S-paper) days to be most memorable, because of a teacher who made me think and challenged me in the subject rather than spoonfeeding.
As you say this is the internet (though from a review of one's postings, one can more or less deduce the truthfulness of one's professed identity, eg. nayr69sg does appear to be a real Singaporean medical doctor who is currently practicing medicine in Canada), but I still routinely ask a new SgForum member's background and current profession (which I noticed you've sidestepped, eg. whether you're currently a Chem private tutor or Chem MOE school teacher, but I'll leave it to you whether you wish to share on this), when I notice unusual posts (eg. if the content of the posts clearly indicate the poster is almost definitely not a JC student, this simple fact can be used to assess the honesty of the person by asking the person's background, and 4/5 times I get the less-than-honest response, "I'm just a neighbourhood JC student lah", ok lor if u say so...), and this (my asking the poster's background), is not so much for measuring dicks, but rather that, if the poster (ie. the person I'm talking to) turns out to not actually be a current JC student (the poster being a JC student is a reasonable initial assumption since this forum is for current JC students to ask me for help), and instead turns out that the poster (ie. any newcomer who responds to my Chem qns or asks me Chem qns) is actually currently an undergrad or post grad or fellow private tutor or MOE school teacher, then it would be wholly inappropriate (rude even) for me to appear condescending and 'talk-down' to the poster (ie. when discussing Chemistry concepts, eg. If I replied you with a "Go google or ask your school teacher on the definition of such-and-such, then get back to me with your revised answer", which would be pedagogically appropriate if you are indeed a JC student, on the other hand would naturally be offensive if you're an undergrad or post grad or fellow private tutor or MOE school teacher, something I'd rather avoid, which is why I ask of the person's background and current profession, and hope to receive an honest response.
Indeed, the 1 out of 5 respondents in past years, a mere handful, did reply me (sometimes through private messaging), to say they are currently an undergrad or post grad or fellow private tutor or MOE school teacher, I appreciated their candour. And it made me all the more willing to help them with their Chem questions, and with more level-appropriate replies, eg. "I'd suggest you advise your students to do it this way...".
All in all, tk2018 (whether you're currently an MOE teacher or private tutor or something else altogether), welcome to SgForums, and you're welcome to join me in advising and helping out Singapore JC students with their questions, although in all honesty, you'll probably be disappointed and bored with this forum, because business is slow (ie. not many JC students ask for help here), despite my sincere hopes that all Singapore JC students who can't afford private tuition, register an SgForums account to receive help with their JC subjects here (other than myself and Chemguide7 for Chemistry, Wee_Ws helps out for Mathematics, Eagle helps out for Physics and Mathematics, and Darkness_hacker99 helps out for Biology, but business (ie. students asking qns) has been so slow in recent years, that these folks only drop occasionally these days, if at all.
tk2018, if you do have your own Chemistry website, or blog, even if it's your own private tuition website, if it contains useful materials for students, not necessarily study notes, can be a collection of links to interesting Chemistry articles etc, feel free to post your url here to share with JC students (from the logged statistics, the vast majority of visitors to this forum are lurkers, and while there are certainly many private tutors and school teachers lurking here, I'll like to think that there are many genuine JC students visiting here as well, and would like to encourage them to register an SgForums account to get help for their A level subjects here, especially if they cannot afford private tuition).
Mr Chong (Chemguide7)'s H2 Chemistry website :
My BedokFunland JC website :
Originally posted by hoay:
Simple molecular structures have intermolceualr forces.
what about Giant covalent sturtucres. Do they have intermolecular forces? they have lots of strong covalent bonds which need very high eenrgy to be broken down.
Except graphite which has VDW forces, in diamond if there are two units of diamond won't they have VDW forces bewteen them?
Markerâ€™s comment : There are still some students who drew mechanism like A --> B --> C --> D, the correct way to draw is A --> B, B --> C, C --> D.
No, that is just totally wrong. Although Cambridge will accept either way for A level purposes, the correct (ie. University) way, and indeed the way preferred by Cambridge markers at A levels, is to draw A --> B --> C --> D.
To draw A --> B, B --> C, C --> D is a terribly inefficient and childish way, which Cambridge tolerates but discourages, even at A levels.
Here's an example of how we draw mechanisms at University levels, and thus also the recommended way for competent (not childish) A level students :
Originally posted by hoay:
In C6H6 the oxidatio number of carbon is -1. In chlorobenzene the oxidation state of Cl is +1 as calculated by the rules of oxidation numbers.
The electrophilic substiution of benzene with chorine to produce chlorobenzene and hydrogen chloride can also be described as Dispropportionation reaction. Is it correct to think like that?
Like wise in case of nitrobenzene the oxidation number of N is +5. When it is reduced N changes to -1.
Why chlorine is +1 in chlorobeznene. Please explain.
The clearest instance of disproportionation in Org Chem would be the Cannizzaro reaction.
When nitrobenzene is reduced to phenylamine, the OS of N decreases from +3 to -3.
"...as calculated by the rules of oxidation numbers..."
Those 'rules' are merely simplified guidelines that are of limited use, and should only be applied at O levels.
The quirkiness about A levels, is that it's caught awkwardly in-between overly-simplified O levels, and the real / correct Uni level Chemistry.
The overly-simplified OS / ON 'rules' will fail when applied to Org Chem and complicated species in Inorg Chem.
To correctly determine the correct OS / ON of an atom, you'll have to consider the structure of the species containing the atom, formal charges and electronegativities, as well as resonance contributors and resonance hybrids (where applicable).
For Org Chem, Cambridge requires the A level student to be familiar with the use of Functional Group Level.
Originally posted by hoay :
the ionic equation for the reduction of nitrobenzene to give phenylamine shows 6e being gained. But you just told that the OS of N changes from +5 to -3 mans it gains 8e.
The ionic equation is given in CIE MS June 2016. Refer to Q.6(a)(i). The link is below:
Based on your explanation that the N's OS in phenylamine is -3 make me to deduce that the OS of the carbon bonded to Nitrogen is +6. carbon loses 2e AND hydrogen loses 6e so a total of 8e BUt the MS shows only 6e that are coming from Hydrogens.
Indeed, it's always good to check the balancing of redox equations using both ionic charges, and OSes, they will always match if done correctly.
When nitrobenzene is reduced to phenylamine, the OS of N decreases from +3 to -3, hence 6 e- is involved in the reduction half-equation.
Originally posted by hoay:
the final picture is now:
the carbon bonded to N in both nitrobeznene and phenylamime is +1.
the carbon bonded to N in both these neither lose or gain electrons.
All Other Carbons in both these have OS of -1.
And the 6 electrons come from the reducing agent involved, for this reaction, can be H2(g)/catalyst or Fe(s)/H+ or Sn2+(aq) or Zn(s), etc. LiAlH4 is not recommended as azo compounds are the major products.
Originally posted by hoay:
what about the side-chain carbon in themethylbenzene?? it has -3 charge.
Originally posted by hoay:
me too...It's 2.05 am in Karachi, Pakistan.
Kindly can you explain why disproportionation occurs? with refernce to the metla ions such as Cu+ and Cl2 with NaOH.
For chlorine, under alkaline conditions disproportionation is favored, while under acidic conditions comproportionation is favored. This is due to the nucleophilic attack of the OH- Lewis base unto the Cl2(aq) molecule under alkaline conditions. Under acidic conditions, the thermodynamic driving factors are Le Chatelier's principle together with the positive entropy change of Cl2(aq) to Cl2(g), made possible by the double protonation of the ClO- Bronsted-Lowry base followed by nucleophilic attack from the Cl- Lewis base.
[Singapore] - A young woman scholar from the Agency for Science, Technology and Research (A*Star) was suspected to have taken her own life at a laboratory early Tuesday (Jan 16 2018) morning. Colleagues of Katarina Chlebikova, working at the Institute of Molecular and Cell Biology (IMCB), said that the 26-year-old Slovakian had been troubled over work and relationship issues before her death. In response to media queries, the police said that they were alerted to the case at 10.44am on Tuesday. Her body was found on the eighth storey of 61 Biopolis Drive, where the institute is located. â€œA 26-year-old woman was found motionless and was pronounced dead by paramedics at scene. Police are investigating the unnatural death,â€� they added. TODAY understands that Chlebikova left behind a note suggesting that she killed herself via nitrogen poisoning.
BedokFunland JC's comments on the chemistry involved :
Nitrogen gas itself is physiologically inert and non-toxic, unlike carbon monoxide. However, deliberately pumping into a room excess nitrogen gas, displaces all other gases from the room, including oxygen. This results in asphyxiation and death from oxygen deprivation, as would occur with carbon monoxide poisoning.
That this method can be used, and has been used, to carry out covert assassinations, is known to agents of intelligence agencies such as the CIA, Mossad, MI6, KGB, etc. In the case of the 26-year-old Slovakian young woman in Singapore, she used this method for committing suicide.
Spiritually and karmically, the state of emotional and psychological distress that drove her to commit suicide, will accompany her into the afterlife, and will pose some difficulty in releasing her consciousness from her post-mortem emotional pain and psychosis, and she may need some time to herself before willing to accept and experience love and forgiveness, for sufficient healing of her psychological trauma to occur, before she can move forward vibrationally, onto the intermissive period proper, where further healing, life review and preparation for her next physical incarnation can occur. She will be supported by her guides & helpers at every step of the way, even if she may not be aware of it through her emotional pain. Rest in peace now, Miss Katarina Chlebikova.
Originally posted by hoay:
For Q.4(a)(iii) the complex given does not show cis-trans. The marking scheme says that its mirror images are superimposable. But how ? I think the mirror images are non-superimposable. when we say non-superimposable we say with reespect to 3 -dimensional arrangement. In 3-dimensional they would be different.
Scientists at Stanford University in the US found that injecting tiny amounts of two drugs directly into a tumour not only kills the original cancer, but also triggers an â€œamazing body-wideâ€� immune reaction which destroys distant cancer cells and all metastatic tumors throughout the entire body.
90% of advanced-stage cancer-ridden mice were completely cured of cancer after a single injection, and 100% of the mice were completely cured of cancer after a 2nd injection.
With this breakthrough approach, the elusive cure for cancer is much closer within reach than ever before. 2018 could be the year in which humanity finds the cure for cancer (assuming big pharma doesn't get to the Stanford researchers first).
For decades, McDonalds has been quietly adding a chemical Polydimethylsiloxane (PDMS) into the oil used for cooking French fries, simply because PDMS reduces oil splattering at high temperatures, making French fries easier to cook.
Now, a research team from Japan have found that PDMS helps hair grow on mice, and they expect the findings to be applicable to human beings as well.
Who knows what else McDonalds or other giant F&B brands, have been adding to our foods too all these years without a full understanding of their biochemical effects, eh?
When equal moles of Xe and F2 are reacted, a solid product is generated. Given the final gaseous pressure is 70% of the initial gaseous pressure, and that the unreacted Xe and F2 are in a 4:3 molar ratio, calculate the formula of the solid product, and draw its structure, using stereochemical formula (ie. wedge-dash diagram).
Compare and explain the relative acidities of the ortho, para and meta positional isomers of nitrophenol.
Draw the curved-arrow electron-flow reaction mechanisms (in both directions) to explain how pH shifts the position of equilibrium between the vanadate(V) ion and the oxovanadium(V) ion.
Due to a horrific medical error, a poor Russian woman was â€™embalmed aliveâ€™, receiving an intravenous infusion of toxic formaldehyde (ie. methanal in H2 Chem, it's so toxic that not even bacteria and fungi decomposers can survive, hence its use as an embalming fluid to permanently preserve dead human bodies) by error, instead of harmless sodium chloride solution. She violently convulsed non-stop, screaming in excruciating agony for 14 hours before dying.
[Thailand] - British woman drugged unconscious and raped.
Originally posted by Ngwengsamowo:
Structural isomerism and stereoisomerism should be considered when answering this question. If a molecule contains two non-identical chiral carbon atoms, four optical isomers exist. How many isomers are there with
â—� molecular formula C7H14O and
â—� a five-membered ring and
â—� a tertiary alcohol group?
A)4 B)5 C)9 D)13
Answer is C)9, WHY?
[Medicine / Chemistry / Biology] - Why is methanol toxic? (eg. even if you don't die, you will become permanently blind in both eyes, after consuming alcoholic drinks adulterated with cheap toxic methanol, sold by profit-seeking criminal syndicates trying to circumvent the heavy tax on drinkable ethanol imposed by governments)