The effects of altered thyroid states on lipid peroxidation, antioxidant capacity, and susceptibility to oxidative stress of rat tissues were examined. Hypothyroidism was induced by administering methimazole in drinking water for 15 days. Hyperthyroidism was elicited by a 10-day treatment of hypothyroid rats with tri-iodothyronine (10 micrograms/100 g body weight). In tissues of hypothyroid rats the lipid peroxidation was not modified, whereas in hyperthyroid rats lipid peroxidation increased in liver and heart but not in skeletal muscle. The glutathione peroxidase activity increased significantly in heart and muscle of hypothyroid rats and in muscle of hyperthyroid rats. The glutathione reductase activity was not modified in tissues of hypothyroid and hyperthyroid rats. In both rat groups the whole antioxidant capacity of tissues decreased, but significantly only in liver and heart. The results obtained studying the response to oxidative stress in vitro indicated that the susceptibility to oxidative challenge was increased in all tissues of hyperthyroid rats and in heart and muscle of hypothyroid animals. These results are explainable in terms of tissue variations in haemoprotein content and/or of antioxidant capacity. Since it has been reported that hypothyroidism offers in vivo protection against free radical damage, we suggest that such an effect could be due to greater effectiveness of cellular defence systems different from antioxidant ones.
We have studied biochemical and functional characteristics of three mitochondrial fractions resolved by differential centrifugation from the liver of rats in different thyroid states. In particular, the relation between cytochrome and antioxidant content of the mitochondria and their oxygen consumption and response to oxidative stress has been investigated. The cytochrome content is greater in the fractions at higher density, whereas the opposite pattern is shown for antioxidant level. These biochemical characteristics seem to determine functional ones. In fact, the fraction at higher density exhibit greater oxygen consumption and smaller capacity for opposing a oxidative stress. A similar dependence of functional characteristics on biochemical ones was found in altered thyroid states. Hypothyroidism is associated with decreased cytochrome content and oxygen consumption and increased antioxidant level and effectiveness in responding to oxidative stress. The treatment of thyroidectomized rats with triiodothyronine leads to reversion of such a pattern. We are inclined to explain the differences in susceptibility to oxidative stress of the mitochondria by a modulation exerted by thyroid hormone, during the normal maturation process, on their cytochrome content. In effect, such a content is able to determine both respiratory characteristics and sensitivity to pro-oxidants of mitochondria. This sensitivity and the decrease of antioxidants, possibly due to free radical production associated with the increased oxygen flux, make the mitochondria less able to respond to an oxidative challenge.
Young rats exposed to the cold (4 degrees C) for 15-25 days exhibit remarkable modifications in their thyroid state and in the mitochondrial population of target organs such as liver. The serum total and free T3 levels more or less doubled (from 77 +/- 7 to 130 +/- 7 ng/100 ml and from 350 +/- 25 to 530 +/- 25 pg/100 ml, respectively) after 2 h of exposure while the serum total T4 levels underwent a limited and transitory increase; mitochondrial alpha-glycerophosphate dehydrogenase activity increased. On re-exposure to room temperature the thyroid state returned to normal. Cold exposure diminished the cellular volumes of hepatic cells, while the successive warm re-exposure increased the number of liver cells. The number of mitochondria per nucleus increased after 5 days of cold exposure and doubled after 10 days (from 1,200 +/- 120 to 2,400 +/- 130), while the mean protein content per organelles exhibited an exactly contrary trend. These results suggest that during cold acclimatization, the thyroid, the thyroid plays a role in inducing an augmentation of mitochondrial membrane surfaces per cell by stimulation of the mitochondrial protein synthesizing mechanism. At present, it is not possible to establish whether these effects are due to transcriptional modifications of the nuclear genome only or, more likely, to a dual action at nuclear and mitochondrial level.
An enhanced luminescence technique was used to monitor the response of liver homogenates stressed with sodium perborate. Rat liver homogenates were subjected to oxidative stress with sodium perborate, and the light signals, generated by a suitable system, containing luminol and compounds producing enhancement of light emission such as sodium benzoate and indophenol, were detected by a luminometer. The intensity of light emission (E) was found dependent on homogenate concentration (C). When C increased, E at first increased as well and, then, decreased rapidly. The graphic expression of this phenomenon resulted as a curve that can be described by the equation: E = a.C/exp(b.C). It is proposed that the a value represents the capacity of the tissue to catalyze the production of .OH radical species. The b value might be related to the capacity of the tissue to scavenge such radicals, since it increases when homogenates are supplemented with antioxidants and decreases when homogenates are treated with prooxidant. The results obtained by supplementing homogenates with iron containing substances, or using model systems, suggest that cell substances catalyzing the luminescent reaction, such as the hemoproteins, are "scavengers" as well as radical producers. The concentration-emission curve obtained with suitable model system is described by the equation: E = a.C/exp(b.Ck). It is suggested that, using the k value, information can be obtained on the relative capacity of hemoproteins and antioxidant systems to interact with .OH radicals.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.