Assign. 1: Question 1 Surname, First Name. a).Glucose m

Assign. 1: Question 1 Surname, First
Name
a).Glucose metabolism is the main source of biological energy used in the sustenance and maintenance
of life processes [1]. In the very first chemical step of this metabolic cycle, glucose molecule is first
transported across the very plasma membrane by an action of facilitative glucose transporter flowing
down and across the physiologically active concentration gradient. Hexokinase is an enzyme present in
the mitochondria which then phosphorylates the glucose molecule to a compound called glucose-6-
phosphate (G6P) [2]. This product (Glucose 6 phosphate) then enters into the glycolytic pathway where
it generates molecules of ATP, NADH and then pyruvate. Glucose 6 phosphate may also enter the
pentose phosphate pathway which plays a very vital role in nucleic acids synthesis (both Ribonucleic
acid and deoxy-ribose nucleic acid) along with the production of NADPH – that assists in regulation of
intracellular homeostasis (redox) and synthesis of lipids.
The biological process is called glycolysis. The end products of glycolysis are two Pyruvate, two
NADH (Nicotinamide adenine dinucleotide) and two ATP (adenosine triphosphate).
In presence of enough amount of oxygen, the pyruvate from glycolysis cycle enters into the
mitochondria and then gets fully oxidized in order to release more molecules of ATP. When amount of
oxygen is very limited, it is seen that pyruvate gets transformed to lactate. Hence, glycolysis is the prime
source of main energy reservoir that is adenosine triphosphate (ATP).
b). Citric acid cycle is pivotal biochemical cycle occurring inside the very matrix of mitochondria.[2]
The first metabolic step of this cycle is a vitally crucial step which fuses the two-carbon acetyl group
(from acetyl CoA) with four-carbon molecules of oxaloacetate to forge an entity of six-carbon molecule-
citrate. Citrate gets converted to its isomer known as isocitrate. In step-three of this cycle, iso-citrate is
totally oxidized, releasing an important five-carbon molecule called alpha ketoglutarate. The CoA then
binds the succinyl group, forming an entity succinyl CoA. This energy that is released in the
phosphorylation process occurring at the minute substrate level (during the biological conversion of the
succinyl group to a reduced form of succinate) forms new ATPs. Step six reaction of the citric acid cycle
is dehydration reaction which changes succinate into fumarate. Next, water is then added to fumarate
during feasibility of step seven, resulting in formation of the malate. Then, the very last step occurring in
the citric acid cycle produces oxaloacetate by the oxidation of malate. Then another NADH molecule is
produced. The major end products of the citric acid cycle are ten NADH molecules, two
FADH2 molecules, two ATP molecules and six Co2.
c). Oxidative phosphorylation happens or takes place as a vital biological event in the inner
mitochondrial membrane [3], very much in contrast with most of the biological(respiratory) reactions of
the citric acid cycle and fatty acid oxidation, which happens to take place in the mitochondrial matrix.
NADH reductase, succinate dehydrogenase, ATP synthetase, complex III and IV cytochrome c oxido-
reductase are the major trans-membrane enzymes catalyzing the electron transport chain and oxidative
phosphorylation in an efficient way after completion of citric acid cycle. The fine mechanism of action
of these highly functional enzymes are critical to the feasibility of this imperative biological process.
d). Oxygen’s function is vital at the very end of reactions occurring in electron transport chain and this is
where the oxygen molecule accepts new electrons while picking up protons to form new molecules of
water. If oxygen is absent or not adequate to accept electrons (a person is breathing in compromised
aerobic sphere for instance), the electron transport chain will cease to function and the ATPs will be no
longer produced by the action of chemiosmosis. Without adequate amount of ATP, cells would not be
able to carry out biological reactions which are important for catabolic process and after persisting for a
period of time, the cells can even die.
References
1. Parhofer KG. Interaction between glucose and lipid metabolism: more than diabetic
dyslipidemia. Diabetes & metabolism journal. 2015 Oct 1;39(5):353-62.
2. Springsteen G, Yerabolu JR, Nelson J, Rhea CJ, Krishnamurthy R. Linked cycles of oxidative
decarboxylation of glyoxylate as protometabolic analogs of the citric acid cycle. Nature
communications. 2018 Jan 8;9(1):91.
3. Zheng X, Boyer L, Jin M, Mertens J, Kim Y, Ma L, Hamm M, Gage FH, Hunter T. Metabolic
reprogramming during neuronal differentiation from aerobic glycolysis to neuronal oxidative
phosphorylation. Elife. 2016 Jun 10;5:e13374.

Assign. 1: Question 2 Surname, First
Name
a). The sequence of events are as follows:-
 End plate potentials (EPPs) are actually the bioelectric voltages that cause depolarization in
the fibers of skeletal muscle acted-in by bio- chemical neurotransmitters [1]. These
neurotransmitters then finds a way to bind to the target postsynaptic membrane which exists
around the nearest neuromuscular junction. These postsynaptic terminals are known as "end
plates" as because they are saucer like in shape and opens in the muscle fibers.
 When the developmental action potential travels down and on reaching the axon of
concerned motor end neuron, the vesicles with neuro-excitatory transmitter (acetylcholine) are
released into the proximal nerve- muscle junction.
 Then, these acetylcholine molecules fixes themselves into the target molecular receptors
which are present on the postsynaptic side.
 End plate potential are chiefly elicited by fixation of acetylcholine molecules into the target
receptors within the post neuronal membrane. Two types of receptors which has been
discovered are: nicotinic, muscarinic.
 When the action potential invokes the chemical release from various acetylcholine vesicles,
the molecules of acetylcholine diffuses out and across the proximal junction that fixes to a
group of nicotinic receptors present on linings of the muscle fiber.
 This process allows the enhanced flux of potassium, sodium ions.
 This leads to excitatory depolarization of the muscle cell membrane known as sarcolemma.
b).Though, the concerned insecticide is designed to kill insects but certain insecticides have an
anticholinesterase property [2], strong enough to induce dreary effects if consumed into human
system. These insecticides can lead to poisoning. That is why the parents should be worried rightly
and a thorough medical checkup must be done immediately before onset of any severe symptoms.
c). Dermal exposure of the cholinesterase insecticide can unfortunately leads to biologically
hazardous nicotinic effects which again depends on the intensity and amount of exposure [3]. Dermal
exposure can progress to symptoms like local twitching which can then cause muscle fasciculation(s)
with signs of weakness. There can be a delayed but very progressive, severe muscular paralysis.
d). Respiratory symptoms such as shortness of breath (dyspnea), wheezing and bronchial problems
can be as seen. Muscarnic effects of insecticide poisoning leads to muscle weakness and medical
emergency such as cardiovascular, respiratory collapse [4]. The human sympathetic and
parasympathetic system can also be equally affected, leading to lacrimation and urinary incontinence.
e). Atropin can be used as an antidote [5]. Large doses of atropine, can block dreary autonomic
effects of anticholinesterase. The medication can be provided in conjunction with a cholinesterase
regenerator drug. An effective airway needs to be critically managed to counter the development of
allergic dyspnea. Assistance with artificial ventilation is of course centralized in accordance with
patient requirements. Seizure precautions, lavage and seizure management is medically necessary and
so is the promotion of good hygiene in the patient. Frequent turning and patient rollover activities on
bed are also integral to the nursing interventions in preventing bed rest complications.
References
1. Zanetti G, Negro S, Megighian A, Pirazzini M. Electrophysiological Recordings of Evoked
End-Plate Potential on Murine Neuro-muscular Synapse Preparations. Bio-protocol. 2018 Apr
20;8:e2803.
2. Vale A, Lotti M. Organophosphorus and carbamate insecticide poisoning. InHandbook of
clinical neurology 2015 Jan 1 (Vol. 131, pp. 149-168). Elsevier.
3. Raabe OG, Al-Bayati MA, Knaak JB. Physiologically based pharmacokinetic modeling to
predict tissue dose and cholinesterase inhibition in workers exposed to organophosphorus and
carbamate pesticides. 2017 Nov 22 (pp. 19-46). CRC Press.
4. Guo-Ross SX, Meek EC, Chambers JE, Carr RL. Effects of Chlorpyrifos or Methyl Parathion
on Regional Cholinesterase Activity and Muscarinic Receptor Subtype Binding in Juvenile
Rat Brain. Journal of toxicology and pharmacology. 2017;1.
5. Huang HS, Lee KW, Ho CH, Hsu CC, Su SB, Wang JJ, Lin HJ, Huang CC. Increased risk for
hypothyroidism after anticholinesterase pesticide poisoning: a nationwide population-based
study. Endocrine. 2017 Sep 1;57(3):436-44.