sample
Haven't found the Essay You Want?
GET YOUR CUSTOM ESSAY SAMPLE
For Only $12.90/page

Skeletal Muscle: Role of L-Carnitine Essay

Instructions: You may work together on this assignment and turn it in as a group or individually. You will need to use resources such as the internet in addition to your textbook and the article to answer all the questions below. Allow enough time to read and thoroughly answer each question – I will be reading your answers very closely!!

General Questions

1.What is the purpose of this study?

The purpose of this study is to find out the effect of L-carnitine on the activities of electron transport chain in young and aged rats.

2.What are the main conclusions of this study?

The conclusion is that carnitine may prevents free radicals mediated mitochondrial membrane damages and increases the electron flow through the electron transport chain and thereby increasing energy production in aged rats.

3.How could this study be improved? This is a very open-ended question; just do the best you can.

In this study in activity assays for complex they measure data in different amount of time. For the complex 1 and 3 the initial rate was monitored for one minute, for the complex 2 for 3 minutes, while for complex 4 it was monitored for 15 seconds. Also, they use a different length for monitoring. For the complex 1 it was 340 nm, for the complex 2 it was 600 nm and for the complexes 3 and 4 it was 550 nm. In the study is not mentioned duration of experiment for control group. In the results authors did not giving data about all experimental groups. Data used in conclusion are not the same with a data in figures

4.Define the following terms:

•Senescence: the organic process of growing older and showing the effect of increasing age.

•mtDNA: mitochondrial deoxyribonucleic acid

•Conditionally essential nutrient: nutrients that must be supplied to the body only under special condition, such as stress, aging or illness.

•Oxidative damage (AKA oxidative stress): physiological stress on the body that is caused by the cumulative damage from free radicals not properly neutralized by antioxidants

•Somatic cells: all body cells of an organism – except the sperm and egg cells.

•Mitosis: the process where a single cell divides resulting in generally two identical cells. Each containing the same number of chromosomes and genetic content as that of the original cell.

•Post-mitotic: occurring after or pertaining to the time following mitosis

•Cardiolipin: any phospholipid having the structure of a bisphosphatidylglycerol present in the muscles of the heart.

5.What is the natural role of L-carnitine in the body? What is D-carnitine, and why can we not use it? L-Carnitine is a naturally occurring amino acid which plays a vital role in the metabolism of fat. It functions as a transporter of fatty acids into the mitochondria, the metabolic furnace of the cell. In the body L-carnitine transport fatty acids from the cytosol into mitochondria during the breakdown of lipids for the generation of metabolic energy. D-carnitine is another form of carnitine stereoisomer. D’carnitine is biologically inactive

6.What was the control solution that was given to the rats? What was the experimental solution(s) that was/were given to the rats?

The control solution was 0.89% physiological saline The experimental solution were L-Carnitine (300 mg/kg body weight for day) dissolves in 0.89% physiological saline

7.What were the ages of the rats and the treatment they received for each of the following groups:

•Group Ia: 3-4 months old. Received 0.89% physiological saline intraperitoneally

•Group IIa: above 24 months old. Received 0.89% physiological saline intraperitoneally

•Group Ib: 3-4 months old. Received L-Carnitine (300 mg/kg body weight for day) dissolved in 0.89% physiological saline for 14 days.

•Group IIb: above 24 months old. Received L-Carnitine (300 mg/kg body weight for day) dissolved in 0.89% physiological saline for 14 days.

•Group Ic: 3-4 months old. Received L-Carnitine (300 mg/kg body weight for day) dissolved in in 0.89% physiological saline for 21 days.

•Group IIc: above 24 months old. Received L-Carnitine (300 mg/kg body weight for day) dissolved in in 0.89% physiological saline for 21 days.

8.What is the purpose of groups Ia and IIa?

They were control groups. Groups that closely resembling the treatment group but not receive L-carnitine.

9.Why were heart and skeletal muscle cells examined rather than, for instance, skin cells or liver cells? Think of how much energy/glucose heart and skeletal cells must go through versus skin or liver cells, and include the terms mitosis and post-mitotic.

The heart muscles, which are responsible for the heart, need a lot of energy for conduction. That means that heart muscle tissue cells have a lot of mitochondria for produce ATP. The skeletal muscles are primarily responsible for maintenance of changes in posture, locomotion of the organism itself, as well as keeping the body temperature by producing heat. Skeletal muscle and heart muscle are a post-mitotic tissue. Since the muscles cells have grown they are not divide anymore. Hence, tissues can potentially persist for a lifetime that is why they are more likely to accumulate damage in our example caused by reactive oxygen species.

10.How are reactive oxygen species (ROS), oxidative damage, and DNA linked? During what cellular process are ROS generated?

The mitochondria constitute the major source of reactive oxygen species (ROS). Mitochondrial complexes 1 and 3 are contributed the most to ROS production. The reactive oxygen species cause oxidative damage to surrounding structures and the particularly to mtDNA because is in close distance to the primary site of ROS production. Oxidation by ROS results in the synthesis of faulty proteins, oxidized lipids, and mtDNA mutations, which may lead to cellular and mitochondrial improper function or dysfunction.

11.In an animal cell (disregard plant cells), in which two organelles do you find DNA? Of these two locations, which DNA is more likely to be damaged by reactive oxygen species? Which DNA is more likely to produce nonfunctional (or partially nonfunctional) proteins?

In animal cells DNA found in nucleus and mitochondria. Mitochondria contain DNA as they are thought to be the result of ancient bacteria entering our cells thousands of years ago and living there, providing energy and thereby being a successful mutation. The mitochondria DNA are most likely to be damaged by ROS as well as produce nonfunctional protein.

Individual Questions:

Figure 1 12.What question(s) are the authors addressing with this figure?

In this figure by giving histogram authors show the specific activity of mitochondrial complex 1 from heart and skeletal mussels of 6 groups of rats before and after supplementation of L-carnitine. Taking into account the deviation data is given with mean +- standard deviation.

13.What conclusion do the authors draw from this figure? Do you agree that the data supports their conclusion?

Authors conclude is that the activity of complex 1 was decreased into 42 % in heart and 43% in skeletal muscle mitochondria’s of aged rats. After supplementation of L-carnitine for 14 and 21 days to aged rats the activity of complex 1 enzyme was found to be increased in heart and skeletal muscle compared to young control rats. A significant increase of complex 1 was observed in 21 days supplementation of carnitine for 73% in heart and 69% in skeletal muscle. There was no change being observed in young rats supplemented with carnitine. There was no change being observed in young. From this histogram is not possible to see exact results for each experimental group. Even though, from information that are visible there is no increase of activity for 69% or 73% in Figure 1. Also, in the results information about group 1b and 2b are not given. I cannot be agree that the data support their conclusion because the data used in conclusion are different from the data in Figure 1.

14.Was dose-dependency on L-carnitine established? If so, what kind of physiological response increased with increasing L-carnitine supplements?

Yes. The dose dependency was present. We can see it in figure 1. Activity of complex 1 increased from day 14 to day 21. Supplementation of L-carnitine to old rats increase the activity of NADH dehydrogenase by itself and as an ingredient for formation of reduced glutathione from oxidized glutathione.

15.Why do rats in group IIa have significantly less activity in complex I than mice in group Ia?

In the group 2a used rat 24 months and older while for group 1a rats 3-4 month old. Both group used as a control group and not exposed to L-carnitine. The group 2a is an example of senescence: decrease in the activity of NADH-dehydrogenase which result in slowing down electron flow from NADH to oxygen in complex 1.

Figure 2 16.What question(s) are the authors addressing with this figure?

In this figure by giving histogram authors show the specific activity of mitochondrial complex 2 from heart and skeletal mussels from 6 groups of rats before and after supplementation of L-carnitine. Taking into account the deviation data is given with mean +- standard deviation.

17.What conclusion do the authors draw from this figure? Do you agree that the data supports their conclusion?

Authors conclude that the activity of complex 2 was decreased into 22 % in heart and 34% in skeletal muscle mitochondria’s of aged rats. After supplementation of L-carnitine to aged rats the activity of complex 2 was almost as activity in young rats. The increase was dose dependent. There was no change being observed in young rats supplemented with carnitine. From this histogram is not possible to see exact numbers for each experimental group. The data partially support their conclusion. The results that mention in discussion are seem the same as in figure 2, but the data used in conclusion are not specific and not mention results of some experimental groups.

18.The authors gave a hypothesis as to why the activity of complex II in older rats greater than the activity of complex I and IV. What is it?

The activity of complex 2 in older rats is greater because all components that used in complex 2 encoded by nuclear DNA while all components of complexes 1 and 4 encoded by mtDNA. Nuclear DNA comparing to mitochondria DNA is more resistant to oxidative stresses since it has additional protection. MtDNA is in proximity to inner mitochondrial membrane where ROS produced highly attackable for free radicals damage. MtDNA does not have self-repairing mechanism. Because of that factors, the mutation rate of nuclear DNA is lower than mtDNA.

19.Look at the activity of complex II in heart cells in group IIb, and compare it to group IIa and IIc. According to the authors’ hypothesis, is the activity level of group IIb where you would expect to be? If not, where would you expect the activity level to fall at, and why?

The activity of group 2b in the complex 2 is a little bit lower than in group 2a and much lower than in group 2c. According to the authors hypothesis the level of activity in group 2b supposed to be higher than in group 2a and lower than in group 2c. I expect it to fall in this interval because supplementation of L-carnitine suppose to increase the activity of complex 2 comparing to control group, but be lower then in group 2c according to dose dependence.

Figure 3 20.What question(s) are the authors addressing with this figure?

In this figure by giving histogram authors show the specific activity of mitochondrial complex 3 from heart and skeletal mussels of 6 groups of rats before and after supplementation of L-carnitine. Taking into account the deviation data is given with mean +- standard deviation.

21.What conclusion do the authors draw from this figure? Do you agree that the data supports their conclusion?

Authors conclude that the activity of complex 3 was decreased into 32 % in heart and 28% in skeletal muscle mitochondria’s of aged rats. After supplementation of L-carnitine to aged rats the activity of complex 3 was almost as activity of the same complex in young rats. The increase was dose dependent on carnitine supplementation. There was no change being observed in young rats supplemented with carnitine. From this histogram is not possible to see exact numbers for each experimental group. Also, in the results any information about group 1b and 2b are not given. The data partially support their conclusion. The results that mention in discussion are seem the same as in figure 2, but the data used in conclusion not specific and results of some experimental groups not mentioned.


Essay Topics:


Sorry, but copying text is forbidden on this website. If you need this or any other sample, we can send it to you via email. Please, specify your valid email address

We can't stand spam as much as you do No, thanks. I prefer suffering on my own