Enhanced oxidative stress in female rat brain after gonadectomy

Kume-Kick, June; Ferris, David C.; Russo-Menna, I; Rice, Margaret E.

doi:10.1016/0006-8993(96)00744-5

Cited by 52 publications

(29 citation statements)

References 47 publications

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“…In animal studies, due to lower enzyme activity levels of SOD and glutathione peroxidase in males, oxidative damage to mitochondrial DNA is 4-fold higher in males compared to females [56] . Oxidative stress, as measured by a loss in tissue ascorbate after cerebral ischemia, is greater in the brain of male animals compared to females [57] . The activity of catalase, an anti-oxidant enzyme, is also higher in females than in males [58] , and estrogen induces glutathione peroxidase activity [59] .…”

Section: Mtd In Autismmentioning

confidence: 95%

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Rossignol¹,

Bradstreet²

2008

American J. of Biochemistry and Biotechnology

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Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernable mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions. Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.

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Section: Mtd In Autismmentioning

confidence: 95%

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Rossignol¹,

Bradstreet²

2008

American J. of Biochemistry and Biotechnology

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“…11,12 In the present study, we investigated the effect of raloxifene treatment on the levels of SOD, GPX, CAT, TrxR activities, MDA and GSH in liver, heart and brain cortex of ovariectomized rats.…”

Section: Introductionmentioning

confidence: 99%

The potential antioxidant effect of raloxifene treatment: a study on heart, liver and brain cortex of ovariectomized female rats

Konyalιoğlu

Durmaz

Yalçın

2006

Cell Biochemistry & Function

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The antioxidant activity of some compounds buffer the free radicals generated either endogenously or exogenously, thus decreasing the potential damage mediated by oxidation. Recent studies documented that raloxifene has antioxidant properties in vitro. However, there are limited animal studies available to show raloxifene's antioxidant properties. We aimed to investigate the effects of raloxifene on antioxidant enzymes such as SOD, CAT and GPX, TrxR and the levels of GSH and MDA in heart, liver and brain cortex of ovariectomized female rats. Female Sprague Dawley rats weighing 300-350 g (n=24) were divided into three groups: (I) Eight non-ovariectomized rats were used as naive controls without any treatment (non-ovariectomized group, n=8). Five weeks after ovariectomy, (II) Ovariectomized placebo group (n=8) was given physiological saline, and (III) Raloxifene group (n=8) was given raloxifene 1 mg/kg sc. daily for 12 days. Ovariectomy induced significant increases on SOD, GPX, CAT activity and MDA levels in brain, heart and liver tissues compared to non-ovariectomized rats ( p<0.05). Raloxifene treatment led to decreased levels of SOD activity in heart, GPX activity in brain and CAT activity in liver tissue when compared to ovariectomized group ( p<0.05) but there was no change in activity of TrxR in all groups. The levels of MDA in brain, heart and liver tissues increased in ovariectomized group when compared to non-ovariectomized rats ( p<0.05). Raloxifene had a significant attenuating effect on the levels of MDA in brain and heart tissues. Our results also indicate that the levels of GSH in brain, heart and liver tissue decreased when compared to non-ovariectomized rats. Raloxifene treatment was observed to significantly increase the levels of GSH in brain and heart tissues ( p<0.05). However, there were insignificant differences for the GSH levels in liver tissues of ovariectomized placebo or raloxifene groups. In conclusion, our results demonstrate that raloxifene may be more effective against oxidative stress in heart and brain than in liver tissue.

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“…Reports about the effect of ovariectomy on antioxidant enzymes and lipid peroxidation are conflicting. Kume-Kick et al indicated that gonadectomy was caused to oxidative stress in brain of female rat and suggested that ovarian sex hormones have protective role in the prevention of oxidative stress [20,21]. Borras et al founded an increase in lipid peroxidation and a decrease in glutathione levels in liver and brain mitochondria of ovariectomized rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of calcitonin on lipid peroxidation in ovariectomized rats

et al. 2010

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KEYWORDSCalcitonin is one of the active substances which is recently used effectively in osteoporosis treatment. In literature there is no information whether calcitonin cause oxidative stress or not. In this study, subcutaneous calcitonin is applied to rats having experimental postmenopausal osteoporosis and the effects of calcitonin on lipid peroxidation and antioxidant system were investigated. Forty-five healthy adult female Swiss albino Wistar rats were used in this study. The rats were divided into three equal groups as control, ovariectomized (Ovx) and ovariectomized+calcitonin (Ovx-CAL). The rats in Ovx and Ovx-CAL were anaesthetized and underwent a bilateral ovariectomy via ventral incision. Ten weeks after ovariectomy, salmon calcitonin (2 IU/kg body weight) was administered via s.c. at a volume of 1 mL per week for 12 weeks to the Ovx-CAL group. At the end of the drug treatment, livers and kidneys of rats were removed and malondialdehyde (MDA) levels and catalase (CAT) activities were determined by biochemical analysis methods. Data were analyzed by one-way ANOVA followed by the post-hoc LSD multiple test. The liver and kidney MDA levels were increased whereas the activity of CAT enzyme was decreased as a result of ovariectomy compared to values in the control group. Similar results were observed in Ovx-CAL group; however, the decline in the CAT activity in the kidney was not significant. In conclusion, we may suggest that calcitonin treatment increases the oxidative stress in osteoporotic rats. OsteoporosisOxidative stress Antioxidant Ovariectomy Calcitonin

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Enhanced oxidative stress in female rat brain after gonadectomy

Cited by 52 publications

References 47 publications

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

The potential antioxidant effect of raloxifene treatment: a study on heart, liver and brain cortex of ovariectomized female rats

Effect of calcitonin on lipid peroxidation in ovariectomized rats

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