Oxidative Stress Induced Age Dependent Meibomian Gland Dysfunction in Cu, Zn-Superoxide Dismutase-1 (Sod1) Knockout Mice

Abstract Superoxide dismutase 1 suppresses oxidative stress within cells by decreasing the levels of superoxide anions. A dysfunction of the ovary and/or an aberrant production of sex hormones are suspected causes for infertility in superoxide dismutase 1-knockout mice. We report on attempts to rescue the infertility in female knockout mice by providing two antioxidants, ascorbic acid and/or coenzyme Q10, as supplements in the drinking water of the knockout mice after weaning and on an investigation of their reproductive ability. On the first parturition, 80% of the untreated knockout mice produced smaller litter sizes compared with wild-type mice (average 2.8 vs 7.3 pups/mouse), and supplementing with these antioxidants failed to improve these litter sizes. However, in the second parturition of the knockout mice, the parturition rate was increased from 18% to 44–75% as the result of the administration of antioxidants. While plasma levels of progesterone at 7.5 days of pregnancy were essentially the same between the wild-type and knockout mice and were not changed by the supplementation of these antioxidants, sizes of corpus luteum cells, which were smaller in the knockout mouse ovaries after the first parturition, were significantly ameliorated in the knockout mouse with the administration of the antioxidants. Moreover, the impaired vasculogenesis in uterus/placenta was also improved by ascorbic acid supplementation. We thus conclude that ascorbic acid and/or coenzyme Q10 are involved in maintaining ovarian and uterus/placenta homeostasis against insults that are augmented during pregnancy and that their use might have positive effects in terms of improving female fertility.

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The Role of 2% Rebamipide Eye Drops Related to Conjunctival Differentiation in Superoxide Dismutase-1 (Sod1) Knockout Mice

Investigative Opthalmology & Visual Science ◽

10.1167/iovs.17-23213 ◽

2018 ◽

Vol 59 (3) ◽

pp. 1675 ◽

Cited By ~ 3

Author(s):

Takashi Kojima ◽

Cem Simsek ◽

Ayako Igarashi ◽

Kazue Aoki ◽

Kazunari Higa ◽

...

Keyword(s):

Superoxide Dismutase ◽

Knockout Mice ◽

Eye Drops ◽

Superoxide Dismutase 1

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Aging and oxidative stress alter DNA repair mechanisms in male germ cells of superoxide dismutase-1 null mice

Biology of Reproduction ◽

10.1093/biolre/ioab114 ◽

2021 ◽

Author(s):

Paulina Nguyen-Powanda ◽

Bernard Robaire

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Dna Repair ◽

Superoxide Dismutase ◽

Germ Cells ◽

Superoxide Dismutase 1 ◽

Male Germ Cells ◽

Dna Repair Mechanisms ◽

Repair Mechanisms ◽

And Oxidative Stress

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.

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Increased Zn/Glutathione Levels and Higher Superoxide Dismutase-1 Activity as Biomarkers of Oxidative Stress in Women with Long-Term Dental Amalgam Fillings: Correlation between Mercury/Aluminium Levels (in Hair) and Antioxidant Systems in Plasma

PLoS ONE ◽

10.1371/journal.pone.0126339 ◽

2015 ◽

Vol 10 (6) ◽

pp. e0126339 ◽

Cited By ~ 6

Author(s):

María Eugenia Cabaña-Muñoz ◽

José María Parmigiani-Izquierdo ◽

Luis Alberto Bravo-González ◽

Hee-Moon Kyung ◽

José Joaquín Merino

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Dental Amalgam ◽

Antioxidant Systems ◽

Superoxide Dismutase 1 ◽

Dental Amalgam Fillings ◽

Amalgam Fillings ◽

Biomarkers Of Oxidative Stress

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Effects of Aging and Oxidative Stress on Spermatozoa of Superoxide-Dismutase 1- and Catalase-Null Mice

Biology of Reproduction ◽

10.1095/biolreprod.116.141671 ◽

2016 ◽

Vol 95 (3) ◽

pp. 60-60 ◽

Cited By ~ 26

Author(s):

J. S. Selvaratnam ◽

B. Robaire

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Superoxide Dismutase 1 ◽

Effects Of Aging ◽

And Oxidative Stress

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Distinct aging-vulnerable trajectories of motor circuit functions in oxidation- and temperature-stressed Drosophila

10.1101/2020.08.19.257832 ◽

2020 ◽

Author(s):

Atulya Srisudarshan Ram Iyengar ◽

Hongyu Ruan ◽

Chun-Fang Wu

Keyword(s):

Superoxide Dismutase ◽

High Temperature ◽

Superoxide Dismutase 1 ◽

Giant Fiber ◽

Motor Processing ◽

Aging Studies ◽

Sensory Motor ◽

Age Dependent ◽

Escape Reflex ◽

The Common

AbstractWe examined several sensory-motor processing circuits in Drosophila across the lifespan and uncovered distinctive age-resilient and age-vulnerable trajectories in their established functional properties. We observed relatively little deterioration toward the end of lifespan in the giant-fiber (GF) and downstream circuit elements responsible for the jump-and-flight escape reflex. In contrast, we found substantial age-dependent modifications in the performance of GF inputs and other circuits driving flight motoneuron activities. Importantly, in high temperature (HT)-reared flies (29 °C), the characteristic age-dependent progression of these properties was largely maintained, albeit over a compressed time scale, lending support for the common practice of expediting Drosophila aging studies by HT rearing. We discovered shortened lifespans in Cu2+/Zn2+Superoxide Dismutase 1 (Sod) mutant flies were accompanied by alterations distinct from HT-reared flies, highlighting differential effects of oxidative vs temperature stressors. This work also establishes several age-vulnerable parameters that may serve as quantitative neurophysiological landmarks for aging in Drosophila.

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