BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: lipids

Smoking Can Harm More Than Just Your Lungs

When you think of the damage smoking does to your body, you think of your lungs, right? Well, did you know that smoking can actually harm your eyes?

Tobacco has previously been proven to be linked to many leading causes of blindness and vision impairments such as cataracts, glaucoma, and macular degeneration, but all of these effects occur in the inner part of the eye. A new study shows that smoking can actually harm and kill cells on the surface of your eyes.

Research from a recent study conducted by Wataru Otus, a biomedical researcher at the Gifu Pharmaceutical University in Japan, and his colleagues, published by Scientific Reports, found that the compounds found in the smoke of cigarettes and smoking devices cause an iron buildup in the corneal epithelium (the outer layer of corneal tissue on the eye), which can harm and kill cells.

In the study, the researchers exposed human epithelium cells to smoke extract of a cigarette as well as that of heated tobacco devices, and recorded their observations. The researchers found that after 24 hours, more cells that were exposed to cigarette and heated tobacco smoke were killed than those not exposed. They also found that smoking tobacco or using heated tobacco devices caused damage to the cells of the outer eye regardless of nicotine or tar being involved.

The cells that were exposed to tobacco products had damaged cell membranes, lumps of iron, and a lot of damaged ferritin, which strongly indicated ferroptosis, a form of programmed cell death.

Ferroptosis human prostate cancer modelFerroptosis occurred when the compounds in the tobacco made contact with the cells on the outer layer of the eye. The compounds caused the ferritin proteins inside the cells – which store and release iron – to break down and release the iron they were storing. Some of the iron that was released bunched up and produced hydroxyl radicals. Hydroxyl radicals are known to be a very reactive species that attacks organic molecules by removing or deteriorating them. In this case, the hydroxyl radicals attacked the lipids in the film on the surface of that eye, an event called lipid peroxidation. When these lipids are attacked and/or destroyed, your eye is much more likely to dry out, because lipids help prevent the eye from drying out due to their role as lubricators. This is why smokers tend to suffer from dry eye syndromeWhen too many radicals accumulate and are damaging the lipids in the cell membranes, cells can die. The death of eye cells (aka photoreceptors) can lead to the loss of or impaired vision.

As a solution in the study, the researchers found that by adding chemicals that are known to block ferroptosis to the human epithelium cells, more cells exposed to tobacco were able to live, suggesting that ferroptosis treatment could help smokers suffering from eye problems.

Moreover, ophthalmologist Dilek Altinörs of the Başkent University in Turkey, who has studied the results of this study, also suggested that smokers experiencing eye problems should use tear drops with ferroptosis blocking compounds. Although, further study needs to be done on the effects and successfulness of this treatment method. 

The findings of the study help one understand how and why it is that cigarette and tobacco devices affect the eyes of smokers, and show treatments for ferroptosis as a possible treatment for smokers’ having eye troubles. But the obviously best way to prevent smoking from harming your eyes is to not smoke at all. Having smokers learn and understand this new information will hopefully show them yet another reason why smoking is harmful, and why it is in their best interest to quit. 

We Didn’t Start the Fire…Gut Microbes Did.

Many scientists have hypothesized that infants’ gut microbiota could influence the development of their immune system. Recently, a test led by Drs. Christine C. Johnson at the Henry Ford Health System in Detroit and Susan Lynch at the University of California, San Francisco, but this theory to test. Specifically, they set out to examine the relationship between an infant’s gut microbiota and their relative risk of atopy and asthma. The researchers inspected the composition of gut microbes in stool samples from almost 300 infants—all part of a diverse study group born in and around Detroit between 2003 and 2007—by means of examining sequence variation within ribosomal RNA. Ultimately, the team found that the infants could be divided into 3 separate groups, each with distinct bacterial and fungal gut microbiota.

When blood samples obtained from the infants at 2 years of age were tested for sensitivity to allergens, the 3 microbiota groups had significantly different risks for allergen sensitivity. The “high-risk” microbiota group had a relatively lower abundance of certain bacteria and a higher level of some fungi, and was more likely to be diagnosed with asthma at 4 years of age. This seeming link between gut microbiota and allergy and asthma was also manifested when other factors associated with allergic disease—such as breastfeeding—were controlled. Moreover, the researchers found that the high-risk group had a distinct set of metabolites that lacked anti-inflammatory fatty acids and breast milk-derived oligosaccharides that were found in children in the low-risk microbiota group, increasing vulnerability to inflammation.

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Neonatal gut microbiota play a huge role in health and disease (Credit: Eric Atkins)

The researchers also mixed immune cells from healthy adult donors in solutions containing metabolites extracted from the infant’s stool samples. The high-risk group’s metabolite samples increased the amount of allergy-promoting immune cells interleukin-4, a cell-signaling protein associated with allergies, and also reduced T-regulatory cells, an essential group of immune cells that suppress allergic responses. This reduction in T-regulatory cells was also spurred by a lipid that the team identified, called 12,13-DiHOME, that was found at high levels in the high-risk group. Discussing this finding, Lynch expressed to The Scientist, “That for me is incredibly exciting as it suggests that microbial-associated metabolites in the neonatal gut may represent an important driver of early-life immune cell phenotypes associated with disease development in childhood.”

The team plans to conduct a similar study that will focus on environmental factors and how they may affect the development of the gut microbiota. According to Lynch, “Understanding the basis of human-microbial development may prove critical to unraveling the basis of allergy and asthma and to developing preventative therapeutic strategies.”

A big hearted snake

Credit: Flickr User Squamata55

For years the scientific community has been fascinated by the phenomena of snakes, such as pythons, eating massive meals at one time and breaking them down slowly over time.  Now thanks to a study by Leslie Leinwand there is an answer to how pythons manage this feat.  After the python eats its organs swell up to two times their size to accommodate this massive amount of digestion.  But what could cause an organ to swell this much?  Leslie and her team have an answer to this as well, fatty acids.  When they drew the snake’s blood after it ate they report that the blood was so filled with fat that it was opaque and it “looked like milk”.  Leslie and her team have not stopped their research here, in fact they learned that when they take three of the fatty acids found in the blood of these pythons and inject them into a living mouse the mouse’s heart will grow just like the pythons did.

This finding lead to another mystery for Leinwand and her team because they are still yet to discover how having large amounts of fat in the blood is harmless to a python while in a human it is incredibly damaging.  In an attempt to get answers Leinwand and her team have injected mice with heart disease with the three fatty acids that lead to heart growth to see if those lipids can have any effects on the condition.  Stay tuned…

The More Chocolate the Better!

Great news for chocolate lovers (of which I am one!)  Keep eating your M&Ms, chocolate chip cookies, and chocolate ice cream!  The more you eat, the healthier your heart….can that be right??!

A recent New York Times article reported that people who ate high quantities of chocolate were less likely to develop cardiovascular disease.  The article reported on a review of research studies published in the British Medical Journal that looked for correlation between chocolate consumption and cardiometabolic disorders.  Seven studies were evaluated – 5 out of the 7 found a positive correlation between high levels of chocolate consumption and decreased risk of disorders such as cardiovascular disease and strokes.  

When I posted a link to this article with great excitement a few weeks ago on Facebook, a few of my skeptical “friends” pointed out that none of the studies, as noted in the Times article, “involved randomized, controlled trials.”  A researcher quoted in the Times article was also cautious, indicating that chocolate should only be eaten in moderation.  What do you think?  How important are “randomized, controlled trials”?  Are you likely to dismiss the concerns and eat your Phish Food a pint at a time?

Currently in AP Biology we are studying organic compounds.  Knowing that saturated fats are associated with clogged arteries and poor cardiovascular health, it would be interesting to find out what kinds of fats are in chocolate.  Perhaps it is not the types of lipids, but instead particular chemicals in chocolate that contribute to heart health.    Sounds like something that should be explored by some interested AP Bio students!

Photo by Cleverocity licensed under Creative Commons Attribution Share-Alike Non-Commercial Generic 2.0

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