NG900

I'm not sure on the bio-mechanics of it all - perhaps its got to do with the build up of pyruvate molecules - but the gist of it is:

Aerobic respiration is more efficient. So it will be conducted when sufficient oxygen is available.

Fermentation will occur when there is not enough oxygen - as it provides an alternate means of re-cycling the NADH molecules.

    God as it provides an alternate means of re-cycling the NADH molecules.

    Sorry, but would you mind explaining a little more about the recycling of NADH? (Like is it something relating to glycolysis and stuff?)

    Thanks.

    • God replied to this.

      NG900
      Yeah sure thing. So in glycolysis - NAD+ is needed. In order to keep doing glycolysis - the body needs a way to convert NADH back into NAD+ - which usually is aerobic respiration. But because there isn't any oxygen - it does fermentation instead.

        God thank you so much for your explanation, it starts making sense now 🙂

        Hello there,
        Can someone please explain to me the process of monoclonal antibodies and how effective this method is when we use it as a treatment for a disease?

        Kind regards 🙂

        chemistry1111
        Hi 🙂
        The template strand only serves as the template for transcription (so this template strand is often from DNA, and is used to transcribe into mRNA). Whereas, the coding strand contains the exact same sequence of nucleotides in the mRNA except for thymine.

        Hope this helps

        5 days later

        hi all! sorry if someone's already asked this question:
        does anyone know if there are solutions available for the 2022 sample bio exam on the vcaa page? and if so where they are located?
        my teacher literally made the class complete it under timed conditions and everything but we can't even correct our work...
        thanks in advance!
        -bw

          bw304 I don't think there are any solutions (VCAA doesn't seem to ever give sample exam solutions for any subject, which is really annoying). You might need to ask your teacher for answers, or see if they can mark it for you.

          Can someone please explain part b of this question from the 2019 VCAA exam? Like i get that the mitochondrial DNA of the girl’s finger bone will be very similar to the mtDNA of her female ancestors, but I dont get why. MtDNA has a high mutation rate but it remains relatively unchanged from one generation to another- can someone pls explain what the concept is behind mtDNA and how that links to this question? Cos the way the edrolo textbook has explained it is kinda contradictory..

          Also can someone explain Q4 from the 2020 VCAA exam’s multiple choice section? How do we know that substrate B is gonna be a competitive reversible inhibitor? I actually thought substrate B wouldn’t even bind to the active site cos its not forming a product 😅 - I’ve been a bit confused with these two questions since yesterday so if someone could help clarify this in detail that’d be great. Thanks so much!

            Smartiestarz

            With the 2020VCAA question - I think the clue is that is says 'an enzyme-substrate complex was formed in each of the three test tubes'. This indicates that both substrates have bound to the enzyme. Then - I think its a matter of trial and error.

            Intuitively, i would expect it to either decrease - or stay the same. Then going through each option:

            Option A) can't be true because - it doesn't make sense. The only way substrate A & B could both bind at the same time would be if B was an allosteric inhibitor - in which case you would expect to see no product. But the option says it would be the same as testube 1. It could be a co-enzyme - but then you would expect test-tube 1 to have no product produced.

            Option B) can't be true because substrate b can form an 'enzyme-substrate complex'. Which means, some of the time it will be bonded to the active site. Hence the rate of reaction would decrease - as it doesn't actually make a product when bound.

            Option C) sounds ok.

            Option D) sounds ok.

            Now I'm not 100% sure on the logic to differentiate between C & D. Looking through my old prac exams from last year - I chose C. I think this is why:
            Whenever an answer says something definite - like ' zero' product produced - I tend to doubt it. Even if it was an irreversible inhibitor - some product (theoretically) would still get produced.

            Apologies for the long-winded response. Maybe someone else can help more.

            Smartiestarz

            Also - Mitochondrial DNA is passed down from mother to child. (Unlike chromosomal DNA which is 50/50 split from mother/father)

            Without reading the article - I presume the time-span was too small to pickup any differences in mitochondrial DNA. It could also be that - due to recent interbreeding between the two species - the girl could have mtDNA of her mother's species. Which might be very different to her father's.

            Hello Smartiestarz!

            Can someone please explain part b of this question from the 2019 VCAA exam? Like i get that the mitochondrial DNA of the girl’s finger bone will be very similar to the mtDNA of her female ancestors, but I dont get why. MtDNA has a high mutation rate but it remains relatively unchanged from one generation to another- can someone pls explain what the concept is behind mtDNA and how that links to this question? Cos the way the edrolo textbook has explained it is kinda contradictory..

            mtDNA does not change from generation to generation as much as nuclear DNA because it does not undergo recombination. It is solely inherited maternally (well... in most cases anyways).

            Think about it like this; suppose you have a deck of cards. Which would result in a more drastic change?

            1. Changing, adding, or taking away a card every now and then.
            2. Shuffling the cards, and replacing half of them from another shuffled deck.

            Scenario 1 would be comparable to spontaneous mutations in mtDNA, and Scenario 2 would be comparable to genetic recombination. Sure, mtDNA may accumulate mutations faster than nuclear DNA, but it is still relatively insignificant when compared to nuclear DNA recombination.


            Also can someone explain Q4 from the 2020 VCAA exam’s multiple choice section? How do we know that substrate B is gonna be a competitive reversible inhibitor? I actually thought substrate B wouldn’t even bind to the active site cos its not forming a product 😅 - I’ve been a bit confused with these two questions since yesterday so if someone could help clarify this in detail that’d be great. Thanks so much!

            This was a bad question. Usually we would not call an inhibitor a "substrate" at all, we would call them inhibitors.

            Basically you had to choose the most plausible option, option C. The other options didn't really have any coherence.

            • Option A - Why does both substrate being able to bind to the enzyme simultaneously result in same product output?
            • Option B - How would product output change if the same amount of substrate is added?
            • Option D - If substrate B was an irreversible inhibitor, then why are the enzyme and substrate B shown as separate for the results of test tube 2?

            Again, the question is pretty bad. Is the experiment under timed conditions? If not, reversible competitive inhibitor shouldn't make a difference in the end... etc.

            Hey! So enzymes increase the reaction rate by lowering the activation energy required for a reaction, I was wondering how enzymes do that? I've read that an example of how they lower the activation energy is by bringing reactants together which reduces the amount of energy they use moving around until they collide, is this the only way that they reduce the activation energy?

              Hello there 🙂
              Can someone please explain to me the process of monoclonal antibodies and how effective this method is when we use it as a treatment for a disease?
              And also, for example, if someone has a transplanted organ, what's the specific type f cell that helps in identifying that organ? (Why does it has to be "helper T lymphocyte" but not other immune cells?
              => I came across that question on a practice exam:
              Transplanting organs such as lung, heart, liver and kidney have become routine operations over recent years. Only the shortage of donors limits the number of transplants that can be performed.
              a. What is the name of the specific type of cell that can identify an organ that has been transplanted?

              Cheers.

                Hi NG900! Let me see if I can be of any help!
                So, firstly, monoclonal antibodies are identical lab-made antibodies produced by plasma cell clones, which can be used as an immunotherapy treatment (antibody therapy). They can be both used to activate the immune response (induce/amplify to treat cancer) or suppress the immune response (prevent or reduce to treat autoimmune diseases). I'm assuming your question is referring to how they work, not the production process, but correct me if I'm wrong.
                Here are some examples of how they can be used in the body (but not limited to):

                Antibody-dependent cell-mediated cytotoxicity - Activation immunotherapy:

                • Bind to cancer cells and interact with immune system cells, particularly NK cells (natural killer cells), causing them to recognise the cancer cell coated in antibodies as foreign.
                • Helps them kill the cancer cells.

                Complement activation - Activation immunotherapy:

                • Bind to cancer cells and interact with complement proteins (remember, these are proteins found in the body that opsonise, cause lysis, and attract phagocytes to invading pathogens).
                • This interaction aids in helping the complement proteins recognise the cancer cells as foreign, creating membrane attack complexes to kill the cells or enhancing the functions of other immune cells.

                Checkpoint inhibition - Activation immunotherapy:

                • Immune checkpoints -> Regulate immune system, and when activated, suppress the immune system. This is important for normal bodily functioning, but cancer cells can secrete molecules that stimulate these checkpoints, reducing the ability for the immune system to recognise and destroy them.
                • Monoclonal antibodies -> Block immune checkpoints, meaning immune system can function at a grater capacity and destroy the cancer cells more easily.

                Cytokine inhibition - Suppression immunotherapy:

                • Cytokines = Messenger molecules used by immune system to coordinate an immune response.
                • Monoclonal antibodies -> Bind to and inhibit cytokines to suppress the immune response.

                B cell and T cell depletion and inhibition - Suppression immunotherapy:

                • They bind to autoreactive (cell that recognises self-tissue/self-antigens as non-self) B and T cells -> This can act as a means of inhibiting these cells, or stimulate other immune cells to destroy these autoreactive B and T cells.

                Now, how effective are monoclonal antibodies in comparison to tradition treatments.

                Cancer treatment (activation immunotherapy):

                • Benefit -> More specific and targeted in attack, unlike traditional treatments (chemo and radiotherapy) that target all rapidly dividing cells (means other cells of the body are impacted, such as hair and cells lining gut - results in hair loss, nausea, etc.) This is due to their variable regions that bind with cancer antigens specifically, meaning their is a lower chance of other cells in the body being effected by the treatments and lower side effects.
                • Benefit -> Can be used to stimulate the immune system to recognise and destroy cancer cells, unlike traditional treatments that directly kill cancer cells.
                • Con -> Still has a wide range of side effects, such as fatigue, fever, nausea, shortness of breath. However, it is still generally less than traditional treatments and does depend on the type immunotherapy being used.
                • Con -> Only available as a treatment for very specific types of cancers, and is still used in conjunction with other traditional treatments.

                Autoimmune disease treatments (suppression immunotherapy):

                • Benefit -> Prevents overall immunodeficiency, which is occurs with traditional treatments that try to reduce the symptoms of the patient by suppressing their whole immune system (immunosuppression). This causes the individual to be more prone to developing cancer and infections. Monoclonal antibodies prevent this because only specific autoreactive cells are being targeted, meaning the rest of immune system can function normally.
                • Cons -> Same as cancer treatment cons. It is still used in conjunction with traditional treatments due to not being widely available, and can have some side effects.

                I hope that helps. Let me know if you were actually asking about the production process of monoclonal antibodies, not their uses (wasn't 100% what you were asking, that's all).

                Now, with your second question, the specific type of cell is indeed helper T lymphocytes. This because these are the cells that are presented with the foreign antibodies by antigen presenting cells (aka dendritic cells, macrophages, and B cells). Obviously, these cells will also identify that their is something foreign in the body, but the helper T lymphocyte is required to actually recognise this and stimulate a specific adaptive immune response against the transplanted organ. Not sure if that makes sense, but that's how I interpret the question and their answer.

                  chimichurri
                  From a chemistry point of view (what I've learnt in VCE chem), enzymes lower the amount of activation energy required for the reaction to take place by weakening the bonds that hold together substrate, which means its much easier for the substrate to break down into its respective products, or for bonds to form between the substrates to form the product. This is because less energy is needed to break weaker bonds, and therefore the reaction rate will increase.

                    Re: Enzymes, _sophiestudies_ Answer is really good!

                    I’d suggest that we don’t really need to know anything more complex than this for VCE - but I think I know what you are talking about with the whole ‘bringing reactants together’.

                    I believe there is a khan academy video where he talked about the reaction between an Alkene and water. (An Alkene being a carbon chain with a Carbon=Carbon double bond in the middle)

                    The enzyme/catalyst moves or bends the hydrogens away from the double bond - allowing for the water molecule to attack it (performing a nucleophilic attack). This - without the catalyst - is harder; because the hydrogens would get in the way of the water molecule. This is called a hydration/addition reaction in Chem.

                    While you don’t need to know that for bio - I found it quite interesting last year.

                    Another example is that of ATP synthase. It acts like a windmill - using the flow of H+ ions to provide energy to attach a phosphate group to ADP - forming ATP.

                    So overall, perhaps:
                    An enzyme lowers activation energy by stimulating conditions favourable to the reaction - and weakening intramolecular forces.