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TA‐65 does not increase telomere length during post‐natal development in house sparrow chicks ( Passer domesticus )
Author(s) -
VangorderBraid Jennifer T.,
Sirman Aubrey E.,
Kucera Aurelia C.,
Kittilson Jeffrey D.,
Kibble Tania M.,
Heidinger Britt J.
Publication year - 2021
Publication title -
journal of experimental zoology part a: ecological and integrative physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.834
H-Index - 11
eISSN - 2471-5646
pISSN - 2471-5638
DOI - 10.1002/jez.2449
Subject(s) - telomere , sparrow , passer , biology , telomerase , keratin , longevity , genetics , andrology , physiology , microbiology and biotechnology , zoology , medicine , dna , gene
Telomeres, protective caps at the end of chromosomes, are often positively related to lifespan and are thought to be an important mechanism of organismal aging. To better understand the casual relationships between telomere length and longevity, it is essential to be able to experimentally manipulate telomere dynamics (length and loss rate). Previous studies suggest that exposure to TA‐65, an extract from the Chinese root Astragalus membranaceus , activates telomerase, lengthens telomeres, increases the growth of keratin‐based structures, and boosts the immune system in adults. However, telomere loss is expected to be greatest during early life but whether TA‐65 has similar effects during this life stage is currently unknown. Here, we experimentally exposed free‐living house sparrow ( Passer domesticus ) chicks to TA‐65 during post‐natal development and examined the effects on telomere length and loss, growth of keratin‐based structures, and a measure of cellular immunity. Contrary to expectation, the growth of keratin‐based structures was reduced in TA‐65 chicks and in the second year of the study, chicks exposed to TA‐65 experienced more telomere loss than controls. Thus, the effects of TA‐65 on telomeres and keratin‐based structures differ across life stages and future research will be necessary to determine the mechanisms underlying these age‐specific effects.