A eukaryotic cell is like a bustling metropolis that generates waste every moment. In reality, the final destination of waste is incineration plant. Our cells also need a similar place to handle metabolic waste and peroxisomes serve as such a site.
Peroxisomes: discovery, proliferation, and morphology
In 1954, Swedish biologist J. Rhodin first discovered many small spherical particles in the kidney cells of mice. These particles had a diameter of only 0.5-1 micrometers and were named microbodies. Since their morphology and size are similar to primary lysosomes, and both organelles coexist in the same group in differential centrifugation, many scholars believed that "microbodies" were merely a type of lysosome at that time. It was not until Christian de Duve used the surfactant Triton WR-1339 to distinguish them, since Triton WR-1339 accumulates in microbodies to temporarily reduce their density. Lysosomes contain acid hydrolases, while organelles containing various oxidases, peroxidases, and catalase were named peroxisomes. The concentration of these enzymes is so high that they form orderly protein crystals in the center.
DNA is not found in peroxisomes, and all the proteins are encoded by nuclear DNA. Membrane proteins Pex3 and Pex16 are synthesized on the endoplasmic reticulum and bud off as small vesicles. Along with Pex19 in cytoplasm, they determine which proteins will be embedded into membrane. Most of the enzymes in matrix are synthesized on free ribosomes, then recognized and pulled in by membrane proteins. Peroxisomes can be synthesized de novo or proliferate by binary fission that is similar to bacteria.
They are widely present in animal and plant cells, but they are particularly abundant in certain cells, especially in liver and kidneys that handle metabolic waste. Their number, morphology and enzymes vary in different species and even in different cells of the individual. External environment also significantly affects them. For instance, if a person is addicted to alcohol, their number and size in liver increase. It is for more effectively breaking down alcohol.
Peroxisomes and oxidation, detoxification
Some toxin can't be broken down by hydrolases, so the critical detoxification task falls on peroxisomes. They use a more aggressive approach where the substrates are oxidized directly. One of the pathways is to convert toxin into a carboxylic acid and decompose it in a beta oxidation. Hydroxyl groups are introduced into hydrocarbons to make them alcohols with help of oxygenases. During two stages of dehydrogenation, alcohol first becomes an aldehyde and finally a carboxylic acid.
R-CH₃ + O₂ + NADPH + H⁺ → R-CH₂OH + NADP⁺ + H₂O
RH₂ + O₂ → R + H₂O₂
R′H₂ + H₂O₂ → R′ + 2H₂O
The highly oxidative byproduct hydrogen peroxide is broken down by catalase into water and oxygen to prevent cell damage.
2H₂O₂ → 2H₂O + O₂
If they are alicyclic or aromatic hydrocarbons, the ring should be opened before further reaction. Oxygen atoms are inserted into their rings to make them reactive epoxides. They then become alcohols in a ring-opening reaction. The next step is dehydrogenation for becoming carboxylic acids.
A Simple Respiratory Chain
Peroxisomes may be ancient organelles. The oxygen that is toxic to early life gradually increased in the atmosphere after photosynthesis. Peroxisomes eliminate oxygen and produce certain metabolites for life. However, the disadvantage is that they waste too much energy. Oxidases and catalase couple into a simple electron transport chain that doesn’t produce ATP. Some energy in organic matter dissipates as heat due to the lack of ATP synthase. Later, mitochondria replaced their function, and couple electron transport chain with ATP synthesis during endosymbiosis. However, peroxisomes have an advantage that they more easily consume excess oxygen to prevent cellular poisoning, as their capacity is proportional to oxygen concentration. Increasing oxygen doesn’t accelerate mitochondria to combust organic matter because the optimal concentration within mitochondria is 2%.
α-Oxidation, β-Oxidation of Very Long-Chain Fatty Acids (C > 23)
Mitochondria and peroxisomes are both organelles that burn fatty acids to generate energy. However, they oxidize fatty acids of different lengths. Very long fatty acids must be shortened in peroxisomes because they can’t pass through the double membrane in mitochondria. A process similar to mitochondrial β-oxidation occurs here, but it differs slightly and usually ceases after several repetitions. Every time, a two carbon units are removed to produce a shortened fatty acid, an acetyl-CoA, and a high-energy compound NADH. These are then transported to the mitochondria for oxidation. FADH₂ is absent and hydrogen peroxide is in here, because FAD is replaced by oxidases and oxygen in accepting electrons and hydrogen.
Mitochondrial β-oxidation can’t handle branched-chain fatty acids, so some undergoes α-oxidation in peroxisomes. The second carbon in main chain is removed so that branch no longer occupies the third carbon. This modification makes them suitable to β-oxidation in mitochondria.
C3 plant photorespiration and the glyoxylate cycle
During seed germination, seedlings can’t obtain energy from photosynthesis. In addition to starch hydrolysis, the stored fats are converted into saccharide for germination and seedling growth by peroxisomes, especially in oil-rich plants such as soybeans and sunflowers. Acetyl-CoA is acquired during β-oxidation. It reacts with glyoxylate to form malate, which then participates in carbohydrate synthesis. This process is impossible in animals.
In addition to converting fatty acids into carbohydrates, peroxisomes also participate in photorespiration. This is akin to a factory repairing its defective products for reuse. Rubisco, much like a flawed machine that can’t distinguish between oxygen and carbon dioxide, so glycolate appears when oxygen is mistakenly added to pentose. Eventually, glycolate becomes glycerate again through a series of biochemical reactions in mitochondria and peroxisomes, and reenters the C3 cycle in photosynthesis.