Arsenic is an environmental toxicant known to be a carcinogen and endocrine disruptor. Maternal exposure to arsenic has been associated with fetus malformation and reproductive disorders in male ...offspring. However, it is unclear the extent to which those effects remain during postnatal development and adulthood. Therefore, this study aimed to investigate the long‐term effects of prenatal arsenic exposure on reproductive parameters of male offspring at peripubertal and adult periods. Pregnant female Wistar rats were exposed to 0 or 10 mg/L sodium arsenite in drinking water from gestational day 1 (GD 1) until GD 21 and male pups were analyzed at postnatal day 44 (PND 44) and PND 70. We observed that some reproductive parameters were affected differently by arsenic exposure at each age evaluated. The body and reproductive organs weights, as well as testicular and epididymal morphology were strongly affected in peripubertal animals and recovered at adult period. On the other hand, the antioxidant genes expression (SOD1, SOD2, CAT and GSTK1) and the endogenous antioxidant system were affected in the testes and epididymides from both peripubertal and adult rats. Finally, an impairment in daily sperm production and in sperm parameters was observed in adult animals. Taken together, our findings show that prenatal arsenic exposure affected reproductive parameters of peripubertal and adult male rats mainly due to oxidative stress. Collectively, those alterations may be affecting fertility potential of adult animals.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Arsenic induces reproductive disorders in pubertal males after prepubertal exposure. However, it is unclear the extent to which those effects remain in testis and epididymis of sexually mature rats ...after arsenic insult. This study evaluated the effects of prepubertal arsenic exposure in male organs of pubertal rats, and their reversibility in adult rats. Male pups of Wistar rats on postnatal day (PND) 21 were divided into two groups (n = 20/group): Control animals received filtered water and exposed rats received 10 mg L‐−1 arsenic from PND 21 to PND 51. At PND 52, testis and epididymis of ten animals per group were examined for toxic effects under morphological, functional, and molecular approaches. The other animals were kept alive under free arsenic conditions until PND 82, and further analyzed for the same parameters. Pubertal rats overexpressed mRNA levels of SOD1, SOD2, CAT, GSTK1, and MT1 in their testis and SOD1, CAT, and GSTK1 in their epididymis. In those organs, catalase activity was altered, generating byproducts of oxidative stress. The antioxidant gene expression was unchanged in adult rats in contrast to the altered activity of antioxidant enzymes. Histological alterations of testis and epididymis tissues were observed in pubertal and adult rats. Interestingly, only adult rats exhibited a remarkable decrease in serum testosterone levels. Prepubertal exposure to arsenic caused morphological and functional alterations in male reproductive organs of pubertal rats. In adult rats, these damages disappeared, remained, get worsened, or recovered depending on the parameter analyzed, indicating potential male fertility disorders during adulthood.
•Rats exposed to arsenic from PND 21 to 51 presented damages in reproductive organs.•Arsenic stimulates overexpression of antioxidant enzyme genes in rat male organs.•Gene expression was not altered in organs of adult rats after arsenic insult.•Prepubertal exposure to arsenic reduced testosterone levels in adult rats.•Pathologies remained present in reproductive tissues of As-exposed rats on PND 82.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Arsenic is a metalloid widely found in the environment in organic and inorganic forms. Exposure to inorganic arsenic forms via drinking water has been associated with an increased incidence of ...negative health effects, including reproductive disorders and dysfunction of the endocrine system. However, the impact of arsenic exposure on female reproductive development is still unclear. Therefore, in the present study, we evaluated the effects of prenatal exposure to arsenic on the initial sexual development and puberty onset, and in the morphology of the female reproductive organs, estrous cycle regularity and fertility parameters during adulthood. To do that, pregnant female Wistar rats were exposed to 10 mg/L sodium arsenite via drinking water from gestational day (GD) 1 until GD 21 and the female offspring was evaluated in different postnatal days. Our results showed that prenatal arsenic exposure induced a decrease of litter weight and morphological masculinization in females at postnatal day 1. Moreover, these females had a delay in the age of puberty onset and alteration in estrous cycle number and length. During adulthood, females from the sodium arsenite group showed an increase in endometrium, myometrium and perimetrium areas, and an imbalance in uterine antioxidant enzyme activity. These animals also presented an increase in post‐implantation loss and reabsorption number, leading to reduced viable fetus number. In conclusion, prenatal arsenic exposure in rats was able to promote female masculinization, alter sexual development and impair reproductive performance.
We evaluated the reproductive effects of prenatal sodium arsenite exposure on female offspring of rats. The treatment promoted reduction of litter weight and morphological masculinization in pups from females at postnatal day 1. Moreover, these females had delayed pubertal onset and alteration in estrous cycle number and length. During adulthood, arsenic‐exposed females showed altered uterus morphometry and antioxidant enzymes activities, and reduced reproductive parameters. In conclusion, prenatal arsenic exposure in rats promoted female masculinization, altered sexual development and impaired reproductive performance.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Eugenol is a phenolic compound found in clove extract and extensively used in traditional medicine. It is unclear whether its intake can cause positive or negative effects on liver morphology and ...physiology in healthy individuals. Thus, we aimed to evaluate liver parameters of rats treated with 10, 20, and 40 mg kg−1 eugenol. After 60 days of treatment, liver samples were collected and analyzed by biometric, histological, biochemical, and oxidative analyses. Our results showed that 10, 20, and 40 mg kg−1 eugenol did not alter body and liver weights, serum and hepatic ALT levels and catalase, glutathione-s-transferase, total, Ca2+, and Mg2+ ATPases activities in treated animals. However, 20 and 40 mg kg−1 eugenol reduced Na+/K+ ATPase pump activity and blood glucose levels. They also increased hepatic glycogen content, superoxide dismutase activity, ferric reducing antioxidant power, and nitric oxide and malondialdehyde levels. Still, 20 and 40 mg kg−1 eugenol caused structural and functional damage to the liver tissue of eugenol-treated rats. We concluded that 10 mg kg−1 eugenol is a safe dose for consumption in long-term treatment for rats. Doses higher than 20 mg kg−1 lead to hepatic damage that can impair vital processes of liver functionality.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
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Arsenic exposure intensifies glycogen nephrosis in diabetic rats Sertorio, Marcela Nascimento; Souza, Ana Cláudia Ferreira; Bastos, Daniel Silva Sena ...
Environmental science and pollution research international,
04/2019, Volume:
26, Issue:
12
Journal Article
Peer reviewed
It is known that either arsenic exposure or diabetes can impact renal function. However, it is unclear how these combined factors may influence kidney functions. Therefore, we evaluated ...morphological, functional, and oxidative parameters in the kidney of diabetic rats exposed to arsenic. Healthy male Wistar rats and streptozotocin-induced diabetic rats were exposed to 0 and 10 mg/L arsenate through drinking water for 40 days. Renal tissue was assessed using morphometry, mitosis and apoptosis markers, mineral proportion, oxidative stress markers, as well as the activity of antioxidant enzymes and membrane-bound adenosine triphosphatases. Arsenate intake altered glucose levels in healthy animals, but it did not reach hyperglycemic conditions. In diabetic animals, arsenate led to a remarkable increase of glycogen nephrosis in distal tubules. In these animals, additionally, the activity of catalase and glutathione
S
-transferase, besides the proportion of Fe, Cu, and K in renal tissue, was altered. Nevertheless, arsenate did not accumulate in the kidney and did not impact on other parameters previously altered by diabetes, including levels of malondialdehyde, Na, urea, creatinine, and apoptosis and mitosis markers. In conclusion, besides the intensification of glycogen nephrosis, the kidney was able to handle arsenate toxicity at this point, preventing arsenic deposition in the exposed groups and the impairment of renal function.
We tested the effects of low- to moderate-intensity resistance exercise training (RT) on the structure and function of pulmonary, right ventricle (RV), and skeletal muscle tissues in rats with stable ...pulmonary artery hypertension (PAH).
After the first monocrotaline (MCT; 20 mg/kg) injection, male rats were submitted to a RT program (Ladder climbing; 55–65 % intensity), 5 times/week. Seven days later rats received the second MCT dose. Physical effort tolerance test and echocardiographic examination were performed. After euthanasia, lung, heart, and biceps brachii were processed for histological, single myocyte, and biochemical analysis.
RT improved survival and physical effort tolerance (i.e., maximum carrying load), mitigated the pulmonary artery resistance increase (i.e., TA/TE), and preserved cardiac function (i.e., fractional shortening, ejection fraction, stroke volume and TAPSE). RT counteracted oxidative stress (i.e., CAT, SOD, GST, MDA and NO) and adverse remodeling in lung (i.e., collapsed alveoli) and in biceps brachii (i.e., atrophy and total collagen) tissues. RT delayed RV adverse remodeling (i.e., hypertrophy, extracellular matrix, collagen types I and III, and fibrosis) and impairments in single RV myocyte contractility (i.e., amplitude and velocity to peak and relaxation). RT improved the expression of gene (i.e., miRNA 214) and intracellular Ca2+ cycling regulatory proteins (i.e., PLBser16); and of pathological (i.e., α/β-MHC and Foxo3) and physiological (i.e., Akt, p-Akt, mTOR, p-mTOR, and Bcl-xL) hypertrophy pathways markers in RV tissue.
Low- to moderate-intensity RT benefits the structure and function of pulmonary, RV, and skeletal muscle tissues in rats with stable pulmonary artery hypertension.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
We evaluated the effects of eugenol on histological, enzymatic, and oxidative parameters in the pancreas, parotid, submandibular, and sublingual glands of healthy male rats.
Twenty-four adult Wistar ...rats were assigned into four groups (n = 6/group). Control rats received 2% Tween-20 (eugenol vehicle), whereas the other animals received 10, 20, and 40 mg kg−1 eugenol through gavage daily for 60 d. Major salivary and pancreatic glands were weighed and preserved fixed for microscopic analysis and frozen for in vitro assays.
Eugenol did not alter glands’ weight and serum amylase activity regardless of the concentration. The highest dose of eugenol caused an increase in pancreatic amylase activity and a reduction of lipase activity from serum and pancreas. Eugenol at 40 mg kg−1 diminished the activity of SOD and FRAP in the submandibular gland and CAT and FRAP in the sublingual gland. However, it did not exert any effect on GST regardless of the gland. Additionally, 40 mg kg−1 eugenol increased MDA levels in pancreatic, parotid, and submandibular glands and NO levels in the sublingual. The concentrations of eugenol induced distinct responses in the glands regarding the activity of Na+/K+, Mg2+, and total ATPase activity. They also affected histomorphometrical and histochemistrical parameters in the submandibular gland only.
Results indicated that 40 mg kg−1 eugenol altered most of the biochemical and oxidatived parameters of digestive glands. Only submandibular glands presented histological changes after eugenol exposure suggesting potential implications for its function.
•Eugenol at 40 mg kg−1 decreased lipase and increase pancreatic amylase activity.•The submandibular gland was more sensitive to the effects caused by eugenol.•In the sublingual gland, eugenol changed only NO levels and Mg2+ ATPase activity.•Eugenol modulates the oxidative profile and ATPases activities in the pancreas.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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•Vaccine using rLPG3 in mice improves the liver enzymatic antioxidant defenses.•rLPG3 + SAP vaccine preserves hepatic architecture and reduces granuloma formation in L. infantum ...chagasi infection.•rLPG3 + SAP vaccine reduces the hepatic parasitism in 99 % in mice infected with L. infantum chagasi.
In this work, we aimed to evaluate the effects of the Leishmania infantum chagasi infection on the liver of vaccinated mice, considering parameters of tissue damage and the inflammatory response elicited by vaccination.
We used recombinant LPG3 protein (rLPG3) as immunogen in BALB/c mice before challenge with promastigote forms of L. infantum chagasi. The animals were separated into five groups: NI: non-infected animals; NV: non-vaccinated; SAP: treated with saponin; rLPG3: immunized with rLPG3; rLPG3 + SAP: immunized with rLPG3 plus SAP. The experiment was conducted in replicate, and the vaccination protocol consisted of three subcutaneous doses of rLPG3 (40 μg + two boosters of 20 μg). The mice were challenged two weeks after the last immunization.
Our results showed that rLPG3 + SAP immunization decreased the parasite burden in 99 %, conferring immunological protection in the liver of the infected animals. Moreover, the immunization improved the antioxidant defenses, increasing CAT and GST activity, while reducing the levels of oxidative stress markers, such as H2O2 and NO3/NO2, and carbonyl protein in the organ. As a consequence, rLPG3 + SAP immunization preserved tissue integrity and reduced the granuloma formation, inflammatory infiltrate and serum levels of AST, ALT, and ALP.
Taken together, these results showed that rLPG3 vaccine confers liver protection against L. infantum chagasi in mice, while maintaining the liver tissue protected against the harmful inflammatory effects caused by the vaccine followed by the infection.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Arsenic is a pollutant widely found in the environment due to natural and anthropogenic sources. Exposure to arsenic forms in drinking water has been related with male reproductive dysfunctions in ...humans and experimental animals at adult age. However, the impact of this pollutant on postnatal reproductive development of male offspring exposed in utero to arsenic is still unknown. Therefore, this study aimed to investigate the effects of prenatal arsenic exposure on the postnatal development of the testes and epididymides of rats, during prepuberty. For this purpose, pregnant female Wistar rats were provided drinking water containing 0 or 10 mg/L sodium arsenite (AsNaO2) from gestational day 1 (GD 1) until GD 21 and the male offspring was evaluated in different periods of prepuberty. Our results showed that prenatal arsenic exposure affected the initial sexual development of male pups, reducing their body weight and relative anogenital distance at postnatal day 1. At different periods of prepuberty, male pups from arsenic exposed dams showed a reduction of body and reproductive organs weights, testosterone levels and testis morphometric parameters. Moreover, these pups presented changes in the expression of SOD1, SOD2, CAT and GSTK1 genes and in the activity of superoxide dismutase, catalase and glutathione s-transferase in the testes and epididymides during prepuberty. Taken together, our results show that prenatal arsenic exposure provoked reproductive disorders in prepubertal male rats, probably due to reproductive reprograming and oxidative stress induced by this pollutant.
•Prenatal arsenic exposure affected rat male reproductive development.•Gestational exposure to arsenic caused reproductive reprogramming in male rats.•Testis and epididymis of prepubertal rats are damaged by prenatal arsenic exposure.•Prenatal arsenic exposure disturbed antioxidant genes and enzymes in male pups.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Studies have shown that exposure to either environmental toxicants or hyperglycemia causes hepatic injuries. However, it is unclear the extent to which their combined exposure may influence liver ...functions. Therefore, we aimed to evaluate morphological and functional hepatic parameters in diabetic rats exposed to arsenic.
Diabetes was induced in male rats by intraperitoneal streptozotocin injection. While healthy and diabetic animals received saline solution (negative control and diabetes control, respectively), other animals received 10 mg/L sodium arsenate (arsenic control and diabetes + arsenic groups, respectively) for 40 days in drinking water. Liver tissue was subjected to antioxidant enzymes analysis, cytokine assay, arsenic determination, and histopathological evaluation. Functional markers of hepatic damage were analyzed using serum samples.
Arsenate exposure reduced the antioxidant enzymes activity in healthy rats, and it worsened the reduction of GST in diabetic animals. Consequently, arsenate-exposed animals showed increased malondialdehyde and carbonyl protein levels, being this increase worsened in diabetes + arsenic animals. Arsenate-exposed groups also showed hepatic inflammatory process with high number of mast cells and TNF-α production mainly in diabetes + arsenic animals. Vascular alterations, such as congestion, bleeding, and hemosiderin deposition were intensified in diabetes + arsenic animals, whereas glycogen storage reduced in these animals.
We concluded that arsenate exposure was able to intensify morphological and functional damages in liver tissue of diabetic animals.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
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