Serotonin modulation in neonatal age does not impair cardiovascular physiology in adult female rats: Hemodynamics and oxidative stress analysis

Pedroza, Anderson Apolonio; Nogueira, Viviane Oliveira; Barros, Monique Assis de Vasconcelos; Freitas, Cristiane de Moura; Alves, José Luiz de Brito; Silva, Aline Isabel da; Costa‐Silva, João Henrique; Lagranha, Cláudia Jacques

doi:10.1016/j.lfs.2015.12.024

Cited by 9 publications

(19 citation statements)

References 47 publications

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“…Our data corroborate with previous studies that demonstrated that Fx during developmental age increases the antioxidant defense in brainstem and heart in adult female rats 52 ; increased mitochondrial respiratory capacity, mitochondrial membrane potential, decreased ROS production, and increased the antioxidant capacity in the cardiac tissue from male rats. 17 Positive modulation of the mitochondrial respiration was also observed in the hypothalamus and skeletal muscle persisting into adulthood of male rats.…”

Section: Effects Of Fluoxetine Treatment In Antioxidant Defensessupporting

confidence: 93%

Neonatal treatment with fluoxetine improves mitochondrial respiration and reduces oxidative stress in liver of adult rats

Simões‐Alves

Silva-Filho

Silva

et al. 2018

J of Cellular Biochemistry

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Recent studies have shown that exposure to fluoxetine treatment induces excessive production of ROS, and alters the antioxidant defense system in various tissues and cell types, mainly the liver. When fluoxetine is administered intraperitoneally, the drug rapidly reaches high concentrations in the liver, has potentially multiple toxic effects on energy metabolism in rat liver mitochondria. The aim of this study was to evaluate the effect of pharmacological treatment with fluoxetine during critical period for development on the mitochondrial bioenergetics and oxidative stress in liver of rat adult. To perform this study, the rat pups received Fx, or vehicle (Ct) from postnatal day 1 to postnatal day 21 (ie, during lactation period). We evaluated mitochondrial oxygen consumption, respiratory control ratio, ROS production, mitochondrial swelling by pore opening, oxidative stress biomarkers, and antioxidant defense in liver of rats at 60 days of age. Our studies have shown, that treatment with Fx during the lactation period resulted in reduced body mass gain, improvement of the mitochondrial respiratory capacity, induced higher mitochondrial resistance to calcium ion preventing the mitochondrial permeability transition pore opening, as well as decreased oxidative stress biomarkers, and increased the SH levels and enzymes antioxidant activities (SOD, CAT, GST) in liver of treated rats at 60 days of age. These findings suggest that pharmacological treatment with fluoxetine during critical period of development result in positive changes in liver of rats, as improvement of the mitochondrial bioenergetics and hepatic oxidative metabolism that persist in adulthood.

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Section: Effects Of Fluoxetine Treatment In Antioxidant Defensessupporting

confidence: 93%

Neonatal treatment with fluoxetine improves mitochondrial respiration and reduces oxidative stress in liver of adult rats

Simões‐Alves

Silva-Filho

Silva

et al. 2018

J of Cellular Biochemistry

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“…Thereafter, the samples were centrifuged, washed three times with ethyl/acetate buffer; then, the final pellet was suspended in 6 M guanidine hydrochloride, incubated for 5 minutes in a water bath at 37°C and read at 370 nm absorbance. 24…”

Section: Evaluation Of Aldehydes Productionmentioning

confidence: 99%

“…Absorbance at 480 nm was determined after 4 minutes. 18,24 2.6.4 | Catalase activity Catalase (CAT) catalyzes the decomposition of hydrogen peroxide into water and oxygen. 25 Catalase activity was measured according to the method described by Aebi.…”

Section: Superoxide Dismutase Activitymentioning

confidence: 99%

Mitochondrial impairment following neonatal overfeeding: A comparison between normal and ischemic‐reperfused hearts

Freitas

Nascimento

Andrade-Silva

et al. 2018

J of Cellular Biochemistry

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Overweight and obesity are established factors underpin several metabolic impairments, including the cardiovascular. Although the diversity of factors involved in overweight/obesity‐induced cardiovascular diseases, mitochondria has been highlighted due to its role in cardiac metabolism. As obesity can be originated in early postnatal life, the current study evaluates the effects of neonatal overfeeding on the cardiac mitochondrial bioenergetics and oxidative balance in rats that underwent an ischemia‐reperfusion insult. Seventy‐two hours after delivery, Wistar rat litters were randomly assigned into the control (C; nine pups per mother) and the Overfed (OF; three pups per mother) groups throughout the lactation period. At weaning, male offspring were fed with laboratory chow ad libitum until sacrifice at 30 and 60 days of life. Mitochondrial heart bioenergetics and oxidative balance showed to be deeply affected by neonatal overfeeding at both ages. Interestingly, after ischemia‐reperfusion insult I/R (Langendorff or mineral oil incubation), most parameters evaluated in OF animals were not influenced by additional ischemic‐reperfusion injury. Our findings demonstrated that suckling overfeeding deregulates cardiac mitochondrial alike to ischemia‐reperfusion insult by disengaging electrical mitochondrial coupling and potentiate oxidative stress, wherein the neonatal overfeeding shows to be so detrimental as I/R. Our findings support the concept that nutritional insults in the critical development periods increase the risk for cardiovascular disease and mitochondria impairments throughout life while oxidative damage change between molecular targets.

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“…Body weights were measured at 7th, 14th and 21st day of life, as well as immediately before euthanasia at 60 days of age. Body weights were recorded using an analytical scale (S‐400 with a capacity of 400 g and a readability of 0.01 g; Braz, Freitas, et al., ; Braz, Pedroza, et al., ; Pinheiro et al., ; da Silva et al., ; da Silva, Braz, Silva‐Filho, et al., ; da Silva, Braz, Pedroza, et al., ).…”

Section: Methodsmentioning

confidence: 99%

“…Recent research has indicated that neonatal exposure to fluoxetine, another SSRI, increases SERT gene expression and protein content in the hypothalamus of animals at 21 and 40 days of life (Pinheiro et al., ). Studies from our laboratory have highlighted that fluoxetine treatment during critical development period improves mitochondrial function and reduces oxidative stress in several tissues (Braz, Freitas, et al., ; Braz, Pedroza, et al., ; Simoes‐Alves et al., ).…”

Section: Introductionmentioning

confidence: 99%

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Silva

Freitas

et al. 2018

Eur J of Neuroscience

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The serotonin reuptake is mainly regulated by the serotonin transporters (SERTs), which are abundantly found in the raphe nuclei, located in the brainstem. Previous studies have shown that dysfunction in the SERT has been associated with several disorders, including depression and cardiovascular diseases. In this manuscript, we aimed to investigate how gender and the treatment with a serotonin selective reuptake inhibitor (SSRI) could affect mitochondrial bioenergetics and oxidative stress in the brainstem of male and female rats. Fluoxetine, our chosen SSRI, was used during the neonatal period (i.e., from postnatal Day 1 to postnatal Day 21-PND1 to PND21) in both male and female animals. Thereafter, experiments were conducted in adult rats (60 days old). Our results demonstrate that, during lactation, fluoxetine treatment modulates the mitochondrial bioenergetics in a sex-dependent manner, such as improving male mitochondrial function and female antioxidant capacity.

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Serotonin modulation in neonatal age does not impair cardiovascular physiology in adult female rats: Hemodynamics and oxidative stress analysis

Cited by 9 publications

References 47 publications

Neonatal treatment with fluoxetine improves mitochondrial respiration and reduces oxidative stress in liver of adult rats

Neonatal treatment with fluoxetine improves mitochondrial respiration and reduces oxidative stress in liver of adult rats

Mitochondrial impairment following neonatal overfeeding: A comparison between normal and ischemic‐reperfused hearts

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

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