Effect constant intake.7 A restricted diet that limits

Effect of tert- Butylhydroquinone in C. elegans

 

Introduction

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Attention
deficit hyperactivity disorder (ADHD) is a brain disorder that causes
hyperactivity, impulsive behavior, and inattention, with it usually appearing
as early as age 3.1 Neurodegenerative diseases occur when the nerve
cells and nervous system lose function over time and leads to death.2
Neurodegenerative diseases, such as Parkinson’s disease, decreases the
cognitive functions and movement of the individual.3 Parkinson’s diseases
effects 60,000 elderly Americans each year that continue to suffer through
their symptoms as there are no treatments or cures.4,5 Yet, the
proper nutritional intake is important for an individual’s cognitive process,
behavior, and neuroendocrine and synaptic development, which can be manipulated
to ease some of the Parkinson symptoms in elderly patients.6 Dietary
interventions have been used as an alternative treatment for ADHD in children,
which is suggested by their physicians.7 A diet that contains an
excessive amount of fats and additives have been shown to interfere with the
neuron functions of the brain by causing increase of hyperactivity or lethargic
behavior.7 It has also been suggested that food additives can worsen
the symptoms of ADHD in children who are more exposed to these food additives
than adults.8

Tert-
Butylhydroquinone (TBHQ) is an additive antioxidant found in fats and oils that
has been shown to have a neurotoxic affect to exposed animals.9 Some
food additives have been regulated and given specific concentrations where they
are deemed safe, there is no regulation or studies that have tested the safety
of the combined effect of multiple food additives together.10 Cholesterol
has been shown to clog the artery walls and decrease the amount of oxygen that
flows throughout the body, effecting the function of the brain as a response.9
TBHQ is found in many of the oils and fats in processed foods and it is
suggested to cause changes of behavior over time with constant intake.7
A restricted diet that limits processed additives, such as TBHQ, improves that
mental health of individuals suffering with ADHD and neurodegenerative
diseases.7,9 Without TBHQ in most of our daily intake, a decrease in
the onset of symptoms of those diagnosed with brain disorders and
neurodegenerative diseases can occur.7,9

            Caenorhabditis
elegans (C. elegans), have been
used as a model animal in many studies because of its short life span and a
nervous system that allows for a detailed study on neurons.11 The
entire genome of the C. elegans has
provided a way to manipulate the genes corresponding to neural and muscular
function, which can lead to advances in human genetics.11 The
structure of the C. elegans is
similar to that of a mammal, with similar internal body parts and has a brain
with the ability to function and learn.11 With a similar internal
structure and neural function to humans, C.
elegans can be used as a model to test the effects of neural deterioration.
This experiment will allow for us to test TBHQ and its effects on health and
longevity.

Since
TBHQ is present in most of the food that we consume and diet affects an
individual’s mental health, more research is needed to understand if the food
additive that preserves food could have a possible link to the neural disorders
and diseases. We hypothesize that TBHQ will affect their defecation rate
because of the affect oils and fats have on the pharynx of the C. elegans, which allows for the opening
of their mouth to digest their food, by lining the walls as it would in the
arteries of a human thus decreasing the life span of the C. elegans.

 

 

Materials and
Methods

 

            For this experiment we tested the
effects of TBHQ on C. elegans. The C. elegans were kept in petri dishes
with different concentrations of TBHQ added to the OP50 and the worms were kept
at room temperature (22°C). There were 50 worms per
group with a total of three groups. The worms were kept in these conditions for
twenty days, the average life span for C.
elegans

            The control group contained 50 worms
total and were fed OP50. The first experimental group was given 5% TBHQ in
OP50. The second experimental group was given 10% TBHQ in OP50. Transferring
the adult C. elegans to new plates
was done daily until the 11th day, when the adults finished laying
eggs. These transfers were done under a microscope using a worm pick that
contained OP50 so that the worm attached to the bottom of the pick.

 

Defecation
Assessment

 

            For the defecation rate assessment,
eggs were transferred onto petri dishes containing 5% and 10% concentrations of
TBHQ in OP50 and the control plate with OP50. They were grown in these
conditions at room temperature (22°C) until they reached four days old. On the
fourth day, a total of six worms per group were assessed by placing one worm
into a 60mm NGM plate with OP50. The worm was then observed for a total of 10
minutes and the contractions that the worm had done as it defecated were
counted. The average contractions for the six worms was taken. The average
defecation rate for each group was calculated by: 600 seconds/ average
contractions.

 

Longevity/
Life Span

 

            The transfer of 50 L4 worms per
group was done on day one with 25 worms per plate (total of 6). The control group
contained OP50, the first experimental group contained 5% TBHQ in OP50, and the
second experimental group contained 10% TBHQ in OP50. Each group was
transferred onto a new plate until the worms stopped laying eggs. As soon as
the worms stopped laying eggs, each live worm was transferred onto a new plate
as they were counted. This transfer counted the number of live worms each day
and was recorded.

 

Results

 

Longevity of the C. elegans observed in the three trials
shows that a higher concentration of TBHQ decreases the life span of the C. elegans

 

 

 

 

 

 

 

 

 

 

Rate of defecation observed
in two trials had shown that C. elegans exposed
to TBHQ had a lower average rate of defecation

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Discussion

 

            This experiment was conducted to
test the impact TBHQ has on the longevity and health on C. elegans. We hypothesized that TBHQ would affect the defecation
of the C. elegans, the defecation
would be slower for those exposed to TBHQ, and the life span would be shorter
of those consuming TBHQ. As we hypothesized, the life span of the C. elegans exposed to TBHQ was shorter;
after the fifth day the C. elegans in
experimental groups one and two were deceased, while those in the control group
had a life span that doubled the experimental groups. The defecation rate of
those exposed to TBHQ was lower than those that consumed OP50, the defecation
contraction that occurred did no have the same frequency as those that were in
the control group.

            The short life span of the C. elegans exposed to TBHQ could have
been because of the toxicity of the butane group that makes up the
preservative.3, 12 The butane group within this preservative is
toxic in high dosages, which was exposed to the C. elegans in OP50.12 The food that the C. elegans normally consume is OP50 and
the introduction of TBHQ in their diet had effected their metabolism as their
digestive tracts weren’t accustomed to the new preservative, which is similarly
seen in humans as well when new foods or a change in diet occurs.13 The
digestive system and the metabolic rate changes in humans when they switch
dietary routines and as C. elegans
are used as model organisms because their bodily functions and responses are
similar to humans, the constipation that was observed was expected.11, 13
Humans experience the same form of constipation or excessive defecation when a
change of diet occurs.13 Chronic constipation in humans has been
shown to lower the quality of life, studies have found that there has been a
decrease of activity of those that experience constipation.14 In the
older population, the study had reported that there was a decrease in the well
being of the patient as they reported changes in their physical activity and
mental health.14 The change in the C. elegans’ diet had led to the constipation, which is seen in the
low defecation rates. This lowered metabolism led to further health
complications, as they were not able to digest the TBHQ that they were
consuming.13, 14

 

Conclusion

 

            The toxicity of the TBHQ in C. elegans will need further research to
confirm if the same toxicity can be seen in humans. The change in diet did have
an impact on the C. elegans, which
can be suggested that continual changes and additives in commercialized foods
can have an impact on the people consuming the products.13 The
effect diets can have on changes in the body was seen with the C. elegans, which can suggest that the
additives and preservatives our bodies are consuming on a daily basis do have
an impact to how we respond to artificial preservatives.13

 

References

 

1
National Institute of Mental Health. Attention Deficit Hyperactivity Disorder.
updated March 2016; accessed 2017 October 27. https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml. 2 National Institute of
Environmental Health Sciences. Neurodegenerative Diseases. accessed 2017
October 27. https://www.niehs.nih.gov/research/supported/health/neurodegenerative/index.cfm. 3 National Center for
Biotechnology Information. PubChem Compound Database. accessed 2017 October
27. https://pubchem.ncbi.nlm.nih.gov/compound/tert-Butlyhydroquinone#section=Top. 4 Jin H, Kanthasamy A,
Ghosh A, Anatharam V, Kalyanaraman B, Kanthasamy AG. Mitochondria- targeted
antioxidants for treatment of Parkinson’s disease: preclinical and clinical
outcomes. Biochim Biophs Acta. 2014 Aug;1842(8):1282-94. 5 Parkinson’s
Association of the Carolinas. Statistics on Parkinson’s Disease accessed 2017
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Grimshaw K, Parker KM, Rose- Zerilli MJ, Holloway JW, Warner JO. The role of
histamine degradation gene polymorphisms in moderating the effects of food
additives on children’s ADHD symptoms. 2010 Sept;167(9): 1108-1115. 9 Maulik
M, Mitra S, Bult- Ito A, Taylor B, Vayndorf E, Behavioral Phenotyping and
Pathological Indicators of Parkinson’s Disease in C. elegans Models. National
Institute of Health. 2017,8: 77. 10 Lau K, Graham- McLean W, Williams DP,
Vyvyan- Howard C. Synergistic Interactions Between Commonly Used Food Additives
in a Developmental Neurotoxicity Test. 2005 Dec;90(1): 178-187. 11 Riddle DL,
Blumenthal T, Meyer BJ, et al., editors. C. elegans II. Cold Spring Harbor
(NY): Cold Spring Harbor Laboratory Press; 1997 accessed 2017 October 27.
12 National Center for Biotechnology Information. PubChem Compound Database.
accessed 2017 November 25. https://pubchem.ncbi.nlm.nih.gov/compound/7843#section=Top. 13 Selhub E, Logan AC,
Bested AC. Fermented foods, microbiota, and mental health: ancient practice
meets nutritional psychiatry. J Physiol Anthropol. 2014;33(1):2. 14 Pinto-
Sanchez MI and Bercik P. Epidemiology and burden of chronic constipation.
Canadian Journal of Gastroenterology. 2011 Oct;25(Suppl B):11B-15B.

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