In the last decade, the role of another gaseous free radical, nitric oxide (.NO) has become apparent. However, it can also be metabolized to form reactive nitrogen intermediates (much as with dioxygen) which can be deleterious to the body, if they damage native biomolecules, or advantageous, when they are used by immune cells like macrophages in the destruction of engulfed bacteria.
A molecular orbital diagram of .NO shows it to have a bond order of 2.5 and one unpaired electron in a π2p* antibonding orbital (hence the notation .NO).
Figure: Molecular Orbital Diagram of NO
Here are some of the relevant reactions of NO and its reactive nitrogen intermediates (RNI):
The high energy electron π2p*can leave on oxidation of NO to form the nitrosyl ion, NO+. The bond order in NO+ is three suggesting strong interactions between the N and O atoms.
.NO (oxidation number of N of +2) is thermodynamically unstable and can disproportionate or dismutate (like superoxide) in a self redox reaction to form nitrous oxide (N2O) and nitrogen dioxide (.NO2), with oxidation number for N of +1 and +4, respectively.
In acidic condition .NO can be oxidized to nitrite (NO2-) which can be protonated to form nitrous acid (HNO2).
Nitrous acid can disproportionate or dismutate to form .NO and the radical .NO2 which can be protonated to ONOOH with a pKa of 6.5.
.NO can react with superoxide (.O2-) faster than any other molecule to form peroxynitrite, ONOO- . .NO and superoxide (.O2-) are both produced by cells during infllammation, leading to increased levels of peroxynitrite.
The O-OH bond in protonated peroxynitrite (ONO-OH) can be cleaved either heterolytically to produce NO3- and H+ (70%) or homolytically to produce the radical .NO2 and the highly reactive .OH free radical (30%).
- The deprotonated form of peroxynitrite (ONOO-) can oxidize organic molecules, especially thiols and CO2. When it reacts with CO2, it can form either NO3- and CO2 (65%) or CO3.- and .NO2 (35%). These latter products can oxidize organic molecules in one electron steps. Peroxynitrite can also oxidize protein, DNA, and lipids.
- .NO2 and peroxynitrite can interact with Tyr side chains in proteins to form nitrated proteins (Tyr-NO2), whose presence reflects inflammation.
Macrophages make use of RNIs in the killing of engulfed bacteria. How does one of humankinds greatest foes, Mycobacteria tuberculosis, the causative agent of tuberculosis, avoid this killing mechanism? It is estimated that the bacteria resides persistently in latent form in 2 billion people. If it becomes activated, it becomes one of the greatest killers. Consider the following table:
Killer Diseases through time (Scientist, June 2, 2003)
|Justinian Plaque (6th centr.)||142 million (on 70% mort)||about 100 mill|
|China Plaque (Bubonic) 3rd Pandemic (1896-1930)||30 milion||12 milion|
|Spanish flu 1918-19||1 billion||21 million|
|Malaria||300-500 mil||1 million|
|TB||8 mill||2 mill|
|AIDS||6 million||3 mill|
People infected with the bacteria but without clinical symptoms must mount a sufficient enough immune response to restrain proliferation of the bacteria, but not enough to clear it from the body. Immune-compromised people (transplant recipients taking anti-rejection drugs or AIDS patients) have more difficulty in holding the bacteria at bay. One immune response mediator which restrains bacterial growth is the soluble protein interferon γ (a protein cytokine released by immune cells). This protein induces synthesis of nitric oxide synthase, producing .NO, which through the reactions listed above, can damage bacterial macromolecules.
Bacteria are "digested" in acidic phagosomes of the macrophage. Nitrite formed in the acid conditions from .NO (generated by inducible NO synthase) forms .NO2 and peroxynitrite which have antibacterial properties (better than anti-Tb drugs). Mutant mice that can not synthesize inducible NO synthase have little defense against the bacteria. Darwin e al. exposed the bacteria to sources of nitrite at pH conditions typical of macrophage phagosomes and found mutants sensitive to the RNIs. The mutations involved protein of the bacterial proteasome, a complex multi-protein complex which proteolyzes unwanted (presumably damaged) cellular proteins.
Bacterial genes encoding proteins associated with the bacterial proteasome seem to confer resistance to the effects of macrophage-inducted RNI production. The macrophage proteasome, like other eukaryotic proteasomes, is a cytoplasmic protein complex which degrades damaged cytoplasmic proteins. Although the mechanism is uncertain, the bacterial proteasome may rid the bacteria of nitrated or otherwise oxidized (damaged) proteins or remove the nitrate and facilitate refolding of the damaged protein.
Peroxynitrite in health and disease
Nitric Oxide Synthases: Structure, Function, and Inhibition
Dr. K's Horse Sense
Everyone has heard about the ketogenic diet by now, “keto” for short. It’s basically a reinvention of the Atkins diet with more emphasis on eating fat. Fasting, starvation and no or low simple carbohydrate diets trigger a higher rate of fat oxidation to spare glucose. In omnivores and dogs, a by-product of fat oxidation is the production of ketones – hence the name.
Even starvation, when body fat is the only fuel, fails to produce significant ketosis in horses
The best diet for EMS horses is similar to ketogenic in that simple carbohydrate intake is very low. However, carb and fat calories are replaced by fiber calories. That very basic fact of equine nutrition and physiology is ignored by a proposal to treat EMS with a ketogenic diet.
Ketones are a by-product of burning fat for energy. The mitochondria can burn either glucose or fat. Fat oxidation is a very slow process compared to glucose. When it can keep pace with energy demands most of the fat is efficiently burned in the Krebs cycle in the mitochondria with very little ketone body production. Ketone production increases proportionate to how quickly fats are being presented to the mitochondria compared to how quickly they can be processed so levels go up when carb intake is low – but not in horses.
Multiple studies such as Rose and Sampson 1982 and Hardy 2003 established a long time ago that ketone generation is not important to horses in a variety of circumstances where ketones rise in humans and mice, from fasting to endurance exercise. The reason for this is multifactorial, including very efficient gluconeogenesis and glucose recycling as well as adaptation to direct burning of acetate in horses.
Ketone bodies are formed from acetate generated during fat metabolism and the first step in their reutilization is to convert them back to acetate. Acetate is also the main product of fiber fermentation in horses and horses can get 60+ % of their energy from acetate. Horses may therefore be burning the extra acetate before it is converted to ketones or very efficiency recycling ketones back to acetate and fat – or both.
Like many descriptions of the human ketogenic diet, the equine keto diet proposes ketones are some highly beneficial metabolic fuel so the more the better. In fact, as above, they are only an indicator of incomplete fat oxidation. It is also claimed as ketones go up insulin goes down because high levels of one inhibit the other. This is not true.
In the ketogenic diet, high levels of ketones indicate high fat oxidation because glucose intake from starch and simple sugars is low. Ketones do not directly inhibit insulin. In fact, a high ketone production from a meal high in medium chain triglyceride fats [see below] lowers glucose but increases insulin. Severe ketosis in diabetic ketoacidosis also induces life-threatening insulin resistance.
The equine keto diet involves feeding timothy, Orchardgrass or alfalfa hay, claiming they are more “nutrient dense”, lower carbohydrate and higher fiber than fescue, brome or bermuda (which is not true), no grain or other supplements except an antioxidant sold by the company proposing this. They found, not surprisingly given the normal physiology of the horse, that horses fed this diet don’t have elevated ketone levels. To correct this they also sell a supplemental direct source of ketones and an oil containing medium chain triglycerides – MCTs (although suggested dose is less than for a human). MCT intake causes higher ketone levels because it does not require a carrier to enter the mitochondria so more gets wasted as ketones. Did I mention these three supplements are also expensive?
My INR Readings Before And After My Second AstraZeneca Jab
I am on long-term Warfarin after a serious stroke.
I also measure my own INR using a simple hand-held meter.
So with all the fuss about the AstraZeneca vaccine and blood clots, I thought I’d do an experiment around my second dose of the vaccine.
I maintained a constant Warin dose of 3.5 mg, which is the daily dose, I have agreed with my GP.
I maintained a reasonably constant diet. That is fairly easy if you’re coeliac and on a long-term gluten-free diet, as I am.
measured my INR every morning.
- April 12th – 2.3
- April 13th – 2.8
- April 14th – 2.8
- April 15th – 2.9
- April 16th – 2.5
- April 17th – 2.3
- April 18th – 2.3
- April 19th – 2.4 – 2nd Jab
- April 20th – 2.2
- April 21st – 2.2
- April 22nd – 2.6
- April 23rd – 2.5
- April 24th – 2.4
- April 25th – 2.7
- April 26th – 3.0
- April 27th – 2.7
- April 28th – 2,5
- April 29th – 3.0
- April 30th – 3.1
- May 1st – 2.9
- May 2nd – No Data
- May 3rd – 2.8
It would appear that the results have been less stable since the second jab.
I am a Control Engineer with a B. Eng. from Liverpool University and I’m not surprised at these results.
It’s just like the bounce you get when the wheel of your car hits a pothole.
I would suggest that more research needs to be done.
Figure 1. Cyclic voltammogram of 1 mM Cu(II)TPMA in 0.1 M MOPS buffer (pH 7.2) on a 0.0314 cm 2 gold disc electrode with different levels of nitrite in solution saturated with N2. Scan rate is 50 mV/s. Inset: structure of Cu(II)TPMA.
Figure 1 shows the structure of Cu(II)TPMA (inset) and the resulting cyclic voltammetry (CV) of Cu(II)TPMA on a gold (Au) electrode in the presence of different levels of nitrite in solution. The reversible peaks in the absence of nitrite correspond to a one electron reduction from Cu(II) to Cu(I) within the complex, and the characteristic catalytic peak in the presence of nitrite indicates that the nitrite is reduced by the Cu(I) species. The CVs observed are similar on platinum (Pt) and glassy carbon electrodes (Figure S1 in the Supporting Information). To detect the NO product, a bulk electrolysis experiment was performed by applying cathodic potentials in a cell that is connected to a chemiluminescence nitric oxide analyzer (NOA) (see experimental details in Supporting Information). We use pH 7.2 3-(N-morpholino)propanesulfonic acid (MOPS) buffer, because at a pH lower than 6, nitrite disproportionation occurs, producing background NO and NO2. At pH higher than 8, we observed that the activity of the catalyst decreases significantly, and nitric oxide is not detected. Figure 2 demonstrates that a low, medium and high flux of NO release can be modulated by applying −0.2, −0.3, and −0.4 V, respectively, to the working electrode (vs. 3 M Ag/AgCl reference electrode).
Special: Update on Garlic and Horses
Garlic has a long history of possible health benefits but its safety has been questioned because other members of the Allium family (i.e. wild onion) are known to potentially cause hemolytic anemia.
In 2005, Pearson et al published a study showing doses above 200 mg/kg (3.2 oz for a 450 kg/990 lb horse) for 71 days could cause “hematologic and biochemical indications of Heinz body anemia, as characterized by increases in Heinz body score (HBS), mean corpuscular volume (MCV), mean corpuscular hemoglobin, platelet count, and serum unconjugated and total bilirubin concentrations and decreases in RBC count, blood hemoglobin concentration, mean corpuscular hemoglobin concentration, and serum haptoglobin concentration.”
Heinz bodies are small bubble-like structures on red blood cells. They form after oxidative damage to hemoglobin. Garlic interferes with an enzyme system that normally protects hemoglobin from oxidative stress.
That dosage had been voluntarily consumed but is larger than would typically be fed as a supplement. I had also had personal experience with hemolytic anemia developing in a barn of horses being fed 1 to 2 kg/day of a commercial feed containing garlic in an undisclosed amount. Anemia resolved upon stopping the feed.
Most recently, Saastamoinen et al reported that 83 days of feeding as little as 32 mg/kg (1/2 ounce daily for a 450 kg/990 lb horse) also caused slight decline in hemoglobin, hematocrit and red blood cell counts compared to matched control horses not fed garlic. Unfortunately, they did not check for Heinz body formation, bilirubin or haptoglobin so it is difficult to draw direct comparisons. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356413/ .
While the changes found by the 3 month study of Saastamoinen et all were relative small, so was the dosage used. Horses will vary in their sensitivity to garlic’s effects but it is clear that doses of garlic much smaller than previously thought may cause red cell changes. If you are feeding garlic long term it is wise to monitor for Heinz body formulation and changes in red cell count and parameters.
21 Responses to A facinating Ted Talk on UV and heart attacks
So does this mean Fluorescent lights are good for you then :P
Another interesting thing, is if you keep a snake or a lizard, you need the UV lamp otherwise it will eventually get sick and die. Why my lizards when I was a young child would eventually just die, as my lamp didn’t have UV.
I think Melanoma is over stated with UV. Maybe Melanoma is more likely because of low UV rather then high? As Vit D is very anti cancer. If Melanoma is UV, why do they also happen on the sole of your feet, or in your intestine or your brain?
Be interesting the wavelengths of CFL compared to LED. How does looking at a computer screen affect your Vit D and also your Pineal gland activation?
NOT ME – but I agree with the premise. We are creatures of the sun. My wife avoids it like the plague (even going so far as to put dark film on the car windows. As I do have a day job that is away from the sun, I enjoy working outside on the weekends. And when I get into the car for the commute, I roll down the window and let the sun shine in!
I’ve never needed much of an excuse to get my kit off and laze about in the sun.
I wish I could stay out in the sun more but I’m one of those people who fry quickly and have never had a good tan. More than 20-30 minutes or so in the sun and I’m done. Must be the Celtic genes, none of the family tans well. My blond sisters all use bottle tanning in the summer. I was the one in the family that had dark aurbon hair – mostly gone now, and what’s left is gray. I have plenty of freckles though, if only they would all join up then it would look like a tan. :-)
From your Feb 20 post – Autism, Sulphate, Sunshine, and Nutrition:
@Jradig: Nitric Oxide too, eh? So that’s three compounds from sun on skin… ( Vit-D, Cholesterol Sulphate, Nitric Oxide). One wonders how many more are made, and not noticed… None of those account for the S.A.D. issue either. Looks like sunlight in general, and “Enough UV” in particular, are very important…
“Let the Sunshine In!”….Those creatures of the dark, those flesh eaters anaerobic microbes, those “Monsters of Cthulhu”, described by H.P.Lovecraft, are becoming visible in these “interesting times” we are living in…
Thanks! h/t installed to posting -)
I’m good for about 20 minutes at high noon, then I’m “bright red with manilla spots” -)
OTOH, I think “folks like us” can likely get what we need from far less UV exposure. So take Vit-D, “we” don’t get rickets nearly as easily as darker folks since we can make a load of Vit-D from not much more than our pale faces sticking out of those large overcoats… I’d expect the same to hold for other skin / solar chemicals.
@Philjourdan & Bloke Down The Pub:
Well, at least now you have a ‘snappy comeback’ at anyone accusing you of goofing off -)
seems rather blindingly obvious to me that natural environmental factors are essential for the proper functioning of the body after millions of years of evolution in that environment. Air composition, sun and other factors are stable(ish) now for at least that amount of time.
NO is one of the cutest signalling molecules. NO is a second messenger and its message is ‘increase blood flow’. So what happens when NO is released and increases blood flow, the increase in blood flow/blood volume moves the NO from where it was generated, lowing signal, and NO reacts with oxy-hemoglobin and is converted to nitrite.
The half-life of NO is variable, depending on blood flow, but its half-life is such that it will not get from skin to anywhere else except another bit of dermis.
You can go to the supermarket and buy Arginine, eating that will raise you arginine levels and increase your steady state levels of NO. Some men (and a few women) swear by its effect on target organs, with respect to blood flow.
The role of NO as an antioxidant was covered by someone I know well. He was told that there was no way that nM NO could stop pM hydroxyl damage, based on maths. So he did the experiments.
Nitric oxide and Fenton/Haber–Weiss chemistry: nitric oxide is a potent antioxidant at physiological concentrations
If ever you want to know what happens when you sell your soul to the Devil, just read the life story of Haber, from WWI to just before WWII.
That’s what we should teach our undergraduates.
@E.M. – This topic reminds me of the Lost in Space episode where Dr. Smith was turned into a Carrot. -)
Please! Don’t talk to me of “Lost In Space Dr. Smith”!
He is likely the reason I don’t have a PhD or MD. Just could not stand the idea of being called “Doctor Smith”….
I’ve still had to cope with that. I’m pondering an online ‘doctorate’ program and have to cope with the emotional baggage. (Kids in my high school taunted me with “Dr. Smith”… as I basically knew everything they did plus a whole lot more plus more than that… it left an emotional scar…)
(Maybe I ought to change my name to Jones… -0
Interesting. For quite a few years now I have been abandoning not so sunny England for a 2 week summer holiday, often in France. All too often either staying out of the sun or and getting slightly burnt. But last summer I went for three weeks and this time determined to take more care and used more sun screen and avoided peak hours, but unlike previous holidays I did sunbathe every day, at first for just half an hour at about 4pm and then built up to longer periods, though always avoiding the 11am to 3pm period.
The net result is that I acquired a light but reasonable sun tan which did not peel and took a long time to fade, unlike previous years. But my biggest surprise was a noticeable improvement in a sense of well being which lasted for several months after my return. At the time I put it down to having had a 3 week break, but now I wonder if NO and vitamin D played a significant part in the effect.
Both the spouse and I are “Anglo Saxon Celts” with pale white skin and red head ancestry. (Her Mother and my Dad plus my Mum was about 1/2 red).
The spouse has S.A.D. Seasonal Affective Disorder.
I got a “Lizard Lamp” for the spouse. It does a lot of UVb and not so much UVa. About 20 minutes a day at about 2 feet seems to ‘fix things’ for her.
I tend to be “in the yard” and often ‘minimally clothed’ whenever possible. This specifically excludes summer between 10 am and 2 pm as I burn to a crisp then… i.e. red welty sunburn.
When in Florida and getting much more sun (though some of it ‘under cloud’) I was much better in several ways (though that takes a posting of its own to sort..)
It would seem that even Celts with the Red Head Gene are benefited by sun. Just not between 10 am and 2 pm in the tropics…
FWIW, I strongly recommend the Lizard Lamp in winter for folks out of the Tropics…
So how long do you think you would need to use the “Lizard lamp” and what wattage? Would you wear shorts and tee shirt and have it in the distance.
So UVB makes Vit D, is UVA the one that causes skin cancer ?
I think another big problem is people wearing sun glasses too. As getting light into the eyes is important too, eg for the Pineal gland and UV as well.
@E.M. – Sorry, when I penned the comment, I was not thinking of you as Dr. Smith! I can see where that would be painful! And Funny!
So is that character the reason you are the antithesis of that character? The last thing (based upon your blog alone) anyone can call you is lazy!
I can’t tell someone else what to do, I can only state what we did. We got a lamp at the pet store. I think it was a 20 ish Watt one. I set it up in an aluminum reflector fixture (Al reflects UV) and took my shirt off. Sitting about 2 feet from it, shining on my back, I got a slight “sunburn” after about 40 minutes of exposure. (All this from memory, so you need to do your own experiments…)
I then used that data point to set guidelines for the spouse. More than 2 feet away and less than 20 minutes. Oh, and do NOT look at the bulb. Not only does it specifically say not to look at it, but UV is not kind to eyes.
This effectively cures her Seasonal Affective Disorder AND gets her Vit-D levels up to normal ranges. (She did not respond to supplements. I’m not sure why. We had the M.D. doing blood tests and the “right kind” of Vit-D was not at the right levels. UV “fixed it”. Yes, we were working with an M.D. on all this. While I like “playing with my metabolism” I also recognize that a trained expert in the subject knows a whole lot more than I do, especially about what can go wrong…)
FWIW, my “test series” with the lamp started at 4 feet for 5 minutes. I proceeded by 25% changes in distance (i.e. one foot changes) and doubling of times until I found that point where I got “just a little too much” on the back. I would not recommend that process for anyone young. I’ve already had a few dozens of “blistering red sunburns” on that particular patch of skin, so a ‘bit of pink’ doesn’t significantly change my skin cancer risk (especially given my age). But for anyone young and not already “at risk”, it’s not a good idea to be getting mild sunburns as a way to measure a light bulb…
This is a smaller lower wattage version of what we got
It specifically says not for people on the package. It is for lizards only. Anyone choosing to use it for people are making their own choice to go “off label” and against recommendations. I looked up the UV spectrum and all prior to using ours. As phosphors chosen by the manufacturer can change over time (folks change lamps and processing methods) any new use and new bulb would need a repeat of the “investigate the spectrum” process. (That is: I have no idea if the present bulbs put out more, or less of UVA UVB UVC… compared to what we have now, so you need to do your own investigate and measure on each new bulb).
It would be best to have a UV bulb designed for people (our UV needs are different from those of Lizards – they die without it and can take “high noon in the desert”. I don’t die and can’t take high noon in the desert for more than 20 minutes – and even then I’m in distress…) but I’ve not found one.
I try to keep the character purged from my memory and have as near to zero impact from it on my life as possible. (Much easier post s or so when it basically faded from the culture).
I am who I am, nobody else, and I’m driven by my own character, not some other.
In short: That was then, this is now.
As for UV emitted by CFL’s: Not good at all. Mercury has a nasty spectral line in the UVC range for Vitamin D production you want UVB. Coating is supposed to suppress the UVC spectral line, but usually has cracks. Try to have another glass pane between the CFL and you.
CFL’s and fluorescent lights also do not have continuous spectra, they are shitty sources of UVB for all I know.
For residents of the glorious EU: Do not hope that you can get Vitamin D on a sunbench. All sunbench lamps sold in the EU must have UVB filters installed. Because of skin cancer risk, and because the public is too stupid to make its own decisions.
Often all these shenanigans by the EU Kommissars have convinced me that they want to actively destroy Europe and kill its population after having robbed them blind.
13 March 2013 at 3:02 am
“So UVB makes Vit D, is UVA the one that causes skin cancer ?”
UVB causes skin cancer in melanin-deficient people, and UVC even more so (more energy rich).
Yeah interesting. I was just interested to know how long would actually burn a person. I know I know its experimental only ) Might give it a go for short periods maybe 10min or so in winter.
Interesting that glass stops UVB. So people are Vit D deficient because of the glass as well.
This looks better then the Vit D tablets, as since its a fat soluble vitamin, it can actually accumulate too much with the tablet. As if if you have a blood test, you are only measuring the blood level, not the load level inside your fat reserves, which could be too high if you take supplements for too long and get Vit D toxicity. This is not possible when you get it from light.
So the tanning salons (from article above) are UVA.
An another interesting thing I think I remember, is that on the skin when UV hits it I think the Vitamin D goes to the surface in the oils of the skin or something, then gets absorbed. So if you wash too much, your washing your Vit D away.
But Melanoma maybe is UVB initiated? But I guess if you don’t get UVB you will die from lack of Vit D )
ICSE WITH SOUVIC
Questions with answer for better performance in ICSE subject wise and chapter wise.
chemistry model paper 1
Q.3. (i) The following reactions are carried out :
Q.19. Ans : - (i) Anhydrous : Hydrated salt when heated lose their water of crystallization and are rendered anhydrous.
Na2CO2.10H2O + Δ → Na2CO3 (anhydrous) + 10 H2O.
(ii) Efflorescence : Hydrated salt when left exposed to atmosphere lose their water of crystallization and crumble down to form a powder. Such salts are known as efflorescent salt and the property is known as efflorescence. Na2CO3.10H2O, on being exposed to atmosphere, loses its water of crystallization and crumbles to form powder.
Chemistry - Organic Chemistry (Solved) By SOUVIC JATI
Question .1. (i) Define the term ‘catenation’.
(ii) Which one of the elements – Li, Be, B, C, O, F, Ne shows the property of catenation
Question .2. (i) State the term for:- Compounds having the same general formula and similar chemical properties.
(ii) Name (a) The compound with – OH and with – COOH as the part of its structure.
(b) Homologue of homologus series with general formula CnH2n from the compounds given: Ethane, Ethene, Ethanoic acid, Ethyne, Ethanol.
Question .3. (i) State the structural formula of ethane.
(ii) Draw the structural formula of the two isomers of Butane. Give the correct IUPAC name of each.
(iii) From the following list, write down the appropriate words to fill in the blanks (a) to (e) below: - Addition, carbohydrates, CnH2n-2, CnH2n, CnH2n+2, electrochemical, homologus, hydrocarbons, saturated, substitution, unsaturated.
The alkane from an (a) ________ series with the general formula (b) __________. The alkanes are (c) __________ (d) __________ which generally undergo (e) ___________ reaction.
Question .4. (i) For each of the compounds (a) Ethane, (b) Vinegar [acetic acid] and (iii) Marsh gas [methane], draw the relevant structural formula. What word is used to describe the above three compounds taken together?
(ii) Draw the structural formula of ethane. What is the feature of the ethane structure which allows ethane to react with chlorine in the way it does.
(iii) Give the correct IUPAC name and the functional group for each of the compounds whose structural formulae are given below:
(b) Question .5. (i) What is the special feature of the structure of : (a) C2H4 (b) C2H2.
(ii) What type of reaction is common to both these compounds?
(iii) Give the name and structural formula of (a) a saturated hydrocarbon, (b) an unsaturated hydrocarbon with a double bond.
(iv) Copy and complete the following sentence: A saturated hydrocarbon will undergo _________ reactions whereas the typical reaction of an unsaturated hydrocarbon is _________.
(v) State the term defined by the following :- Compounds containing carbon and hydrogen only.
(vi) State the general formula for a saturated hydrocarbon and give one example and structural formula of the same.
(vii) Draw the structural formula of ethyne. How does the structure of alkynes differ from that of alkenes.
(viii) Fill in the blanks with the correct words : – Alkanes are the (a) _______ [analogous / homologous] series of (b) _______ [saturated / unsaturated] hydrocarbons. They differ from alkanes due to the presence of (c) _________ [double / single] bonds. Alkenes mainly undergo (d) ________ [addition / substiution] reactions.
Question .6. (i) Which compound is heated with soda lime to obtain C2H6 in the laboratory . Write the equation for the same.
(ii) Write the equation for the preparation of CH4 from anhydrous sodium ethanoate [sodium acetate]. Question .7. (i) What type of reaction has taken place between ethane and chlorine.
(ii) Write the equation of the complete combustion of ethane.
(iii) What is the type of reaction taking place between ethane and chlorine to form mono-chloro-ethane.
(iv) Write the equation for the preparation of carbon tetrachloride from methane.
(v) Write a balanced equation for the reaction of ethane and oxygen in presence of molybdenum oxide.
Question .8. (i) Name a solid used instead of conc. H2SO4to prepare ethylene by the dehydration of ethanol.
(ii) Write the equation for the preparation of ethylene from ethyl alcohol. Or, Write the equation for the reaction of heating ethanol at 170ºC in the presence of conc. H2SO4.
Question .9. (i) Write a balanced equation for the reaction between ethene and hydrogen.
(ii) State what do you observe when ethene is bubbled through a solution of bromine in tetrachloromethane (carbon tetrachloride).
(iii) The reaction between ethene and chlorine forms only one product. Name the type of this equation.
(iv) Ethylene forms an addition product with Cl2. Name the product and give its structural formula.
Question .10. (i) Write down the equation for the preparation of ethyne from calcium carbide.
(ii) Burning of acetylene (ethyne) in oxygen produces a very hot flame. What is this hot flame used for.
(iii) State one use of acetylene.
Question .11. (i) What is the type of reaction between ethene and chlorine.
(ii) What feature of the ethene structure makes such a reaction possible.
(iii) Name the product of the reaction between ethene and chlorine.
(iv) What is the special feature of the structure of ethyne.
(v) Ethanol can be converted to ethene which can then be changed to ethane. Choose the correct word or phrase from the brackets to complete the following sentences : -
(a) The conversion of ethanol to ethene is an example of ______ (dehydration / dehydrogenation).
(b) Converting ethanol to ethene requires the use of ________ (concentrated hydrochloric acid / concentrated nitric acid / concentrated sulphuric acid).
(c) The conversion of ethene to ethane is an example of _______ (hydration / hydrogenation).
(d) The catalyst used in the conversion of ethene to ethane is commonly ________ (iron / nickel / cobalt).
(vi) From the list given : - ethanol, ethane, methanol, methane, ethyne and ethene. Name a compound : -
(a) Formed by the dehydration of ethanol by concentrated sulphuric acid.
(b) Which will give a red precipitate with ammoniacal cuprous chloride solution.
(c) Which forms methanoic acid on oxidation in the presence of copper at 200ºC.
(d) Which has vapour density 14 and turns alkaline KMnO4 green.
(e) Which forms chloroform on halogenation in the presence of sunlight.
(f) Which decolourises bromine solution in carbon tetrachloride.
(vii) Write balanced equations for the preparation of the following : -
(a) Ethane from sodium propionate (b) Ethene from ethanol. (c) Ethyne from calcium carbide. (d) Ethanoic acid from ethane.
(viii) Name a reagent which can be used to distinguish between Ethane and ethene.
(ix) Write the equation for the preparation of ethylene from ethyl alcohol.
(x) Name a compound which will give acetylene gas when treated with water.
(xi) Write the equations for the following laboratory preparations : -
(a) Ethane from sodium propionate. (b) Ethene from Iodoethane. (c) Ethyne from calcium carbide. (d) Methanol from Iodomethane.
(xii) Draw the structural formula of a compound with two carbon atoms in each of the following cases : - (a) An alkane with a carbon to carbon single bond.
(b) An alcohol containing two carbon atoms.
(c) An unsaturated hydrocarbon with a carbon to carbon triple bond.
A MAN WITHOUT CHARACTER LEADS OUR NATION. WE TRUST THIS FELLOW TO PROTECT BHARATMATA.
HOW DOES THIS PATHETIC GUJARATI FELLOW KNOW ALL THIS ?
GUJJU NO 2 IS THE FELLOW WHO WROTE A BOOK ON CLIMATE CHANGE-- SPONTANEOUS KNOWLEDGE FELL ON HIS HEAD.
WHY BLAME IGNORANT TAMILS ?
HOW DID ROTHSCHILD MAKE THE HINDU SELF LOATHING
WELL HE COOKED UP TEXTS, HE POISON INJECTED TEXTS
ALL SANSKRIT SRUTIS AND SMRITIS WERE PENNED DOWN IN 5000 BC-- A THOUSAND YEARS BEFORE RIVER SARASWATI DRIED UP..
ALL VEDIC SANSKRIT TEXTS 4 VEDAS , 108 UPANISHADS CAME DOWN ORAL ROUTE FOR 330 CENTURIES BEFORE BEING PENNED DOWN 70 CENTURIES AGO..
WANNA KNOW SOME OF THE COOKED UP/ POISON INJECTED TEXTS ?
WANNA KNOW HOW OLD SANATANA DHARMA IS BY ARCHAEOLOGY ?
SOMEBODY ASKED ME -- COULD YOU REVEAL SOME POISON INJECTIONS IN TAMIL AGAMA DHARMA SHASTRAS --PROPAGATED BY FAKE KANCHI MUTT .