Chemistry, asked by Lonewolf4506, 5 months ago

Differences between rust and production of melanin in their process

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Answered by kiamotors235
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Ultraviolet (UV) radiations alter a number of metabolic functions in vivant. They produce damages to lipids, nucleic acids and proteins, generating reactive oxygen species such as singlet oxygen (O2), hydroxyl radical (HO) and superoxide anion (O2-). Plants and animals, after their water emersion, have developed biochemical mechanisms to protect themselves from that environmental threat through a common strategy. Melanins in animals and flavonoids in plants are antioxidant pigments acting as free radical scavenging mechanisms. Both are phenol compounds constitutively synthesized and enhanced after exposure to UV rays, often conferring a red-brown-dark tissue pigmentation.

Noteworthy, beside anti-oxidant scavenging activity, melanins and flavonoids have acquired secondary functions that, both in plants and animals, concern reproductions and fitness. Plants highly pigmented are more resistant to biotic and abiotic stresses. Darker wild vertebrates are generally more aggressive, sexually active and resistant to stress than lighter individuals. Flavonoids have been associated with signal attraction between flowers and insects and with plant-plant interaction. Melanin pigmentation has been proposed as trait in bird communication, acting as honest signals of quality.

This review shows how the molecular mechanisms leading to tissue pigmentation have many functional analogies between plants and animals and how their origin lies in simpler organisms such as Cyanobacteria. Comparative studies between plant and animal kingdoms can reveal new insight of the antioxidant strategies in vivant.

Keywords: antioxidant strategy, pigments, horizontal gene transfer (HGT); plants, animals, metabolism, genetic bases, mutants.

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Introduction

Ultraviolet (UV) rays are electromagnetic radiations with a wavelength from 10 to 400 nm. The UV radiations are produced by the sun and part of them, those between 290 and 400nm, reach the Earth's surface. UV-C (from 280 to 100 nm) and short UV-B (from 315 to 280 nm) are strongly harmful for vivant life and only the presence of the ozone layer has allowed the development of the life on Earth. Before the formation of the ozone layer, the Earth's surface was subjected to a high level of UV radiations and the life was permitted in aquatic environments only, since water acts as UV filter 1.

UV are the major exogenous source of Reactive Oxygen Species (ROS) such as hydrogen peroxide (H2O2), superoxide radical (O2-), hydroperoxyl (HO2·) and singlet oxygen (1O2) 2. The occurrence of one unpaired electron results in high reactivity of these species due to their affinity to donate or receive an electron to attain stability. The balance between the presence of both pro-oxidants and antioxidants is tightly regulated and extremely important for maintaining vital cellular and biochemical functions. Changing the balance towards an increase in the pro-oxidant over the capacity of the antioxidant is defined as oxidative stress.

UV-B can produce either direct or indirect damages to living organisms. The absorption of photons of UV-B radiations can directly damage the DNA molecules breaking their chemical bonds. The unbounded base interacts with adjacent bases on the same DNA strand to create new bonds and forming dimmers between two adjacent pyrimidines (cytosine and/or thymine) on the same DNA strand. The two major DNA lesions induced by UV-B radiation are CPDs (cyclobutane pyrimidine dimers) and 6-4PPs (pyrimidine (6-4) pyrimidone photoproducts). Occasionally, the lesions within the DNA interfere with the proper translation of a gene, altering or impairing its function. Accumulation of mutations in key genes due to chronic exposure to UV can lead to the development of skin cancer 3. Beside DNA damage, exposure to UV radiations can also produce indirect effects, leading to lipid peroxidation (oxidations of polyunsaturated fatty acids), oxidations of amino acids, as well as oxidative inactivation of specific enzymes by oxidation of their co-factors .

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