Acute exposure to fungicide fluazinam induces cell death in the midgut, oxidative stress and alters behavior of the stingless bee Partamona helleri (Hymenoptera: Apidae).

Stingless bees (Hymenoptera: Meliponini) are pollinators of both cultivated and wild crop plants in the Neotropical region. However, they are susceptible to pesticide exposure during foraging activities. The fungicide fluazinam is commonly applied in bean and sunflower cultivation during the flowering period, posing a potential risk to the stingless bee Partamona helleri, which serves as a pollinator for these crops. In this study, we investigated the impact of acute oral exposure (24 h) fluazinam on the survival, morphology and cell death signaling pathways in the midgut, oxidative stress and behavior of P. helleri worker bees. Worker bees were exposed for 24 h to fluazinam (field concentrations 0.5, 1.5 and 2.5 mg a.i. mL-1), diluted in 50 % honey aqueous solution. After oral exposure, fluazinam did not harm the survival of worker bees. However, sublethal effects were revealed using the highest concentration of fluazinam (2.5 mg a.i. mL-1), particularly a reduction in food consumption, damage in the midgut epithelium, characterized by degeneration of the brush border, an increase in the number and size of cytoplasm vacuoles, condensation of nuclear chromatin, and an increase in the release of cell fragments into the gut lumen. Bees exposed to fluazinam exhibited an increase in cells undergoing autophagy and apoptosis, indicating cell death in the midgut epithelium. Furthermore, the fungicide induced oxidative stress as evidenced by an increase in total antioxidant and catalase enzyme activities, along with a decrease in glutathione S-transferase activity. And finally, fluazinam altered the walking behavior of bees, which could potentially impede their foraging activities. In conclusion, our findings indicate that fluazinam at field concentrations is not lethal for workers P. helleri. Nevertheless, it has side effects on midgut integrity, oxidative stress and worker bee behavior, pointing to potential risks for this pollinator.

Effect of Induced Pulmonary Arterial Hypertension on Testicular Parameters of Wistar Rats Subjected to Resistance Exercise Training.

Pulmonary arterial hypertension (PAH) is characterized by elevated arterial pressure and vascular resistance. PAH may cause alterations in the microcirculation of several organs, including the kidney, liver, brain, and testes. However, it remains unclear whether monocrotaline-induced PAH exerts detrimental effects on animal testes. Thus, we analyzed the impact of PAH on testicular morphology and function. Additionally, we investigated the effect of resistance exercise training (RT) on testicular parameters in PAH rats. Eight healthy Wistar rats and eight PAH rats were subjected to RT training for 30 days; the other PAH and healthy rats (n = 8/group) did not exercise. PAH rats had lower reproductive organ weight, serum testosterone levels, testicular glucose, and nitric oxide (NO) levels, Leydig cell parameters, tubular morphometry, germ cell counts, and daily sperm production than healthy animals did. The practice of RT attenuated the negative impact of PAH on the relative weights of the testes and epididymides, Leydig cell number, nuclear volume, testicular NO levels, and seminiferous epithelium architecture. Moreover, RT positively influenced testosterone levels in PAH animals. We conclude that PAH exerts deleterious effects on testicular histology and function. However, RT can be beneficial to the PAH-affected testicular parameters.

Protective immunity triggered by ectonucleoside triphosphate diphosphohydrolase-based biopharmaceuticals attenuates cardiac parasitism and prevents mortality in Trypanosoma cruzi infection.

Chagas disease is a potentially fatal infection in 21 endemic Latin America countries for which the effectiveness of reference antiparasitic chemotherapy is limited. Thus, we developed three biopharmaceuticals and evaluated the effectiveness of different immunization strategies (recombinant protein NTPDase-1 [rNTPDase-1], DNA plasmid encoding Trypanosoma cruzi NTPDase-1 [TcNTPDase-1] and DNA-NTPDase-1 prime/rNTPDase-1 boost [Prime-boost]) based on the surface ecto-nucleoside triphosphate diphosphohydrolase (ecto-NTPDase) enzyme of T. cruzi in animals challenged with a virulent strain (Y) of this parasite. BALB/c mice were immunized three times at 30 days intervals, challenged with T. cruzi 15 days after the last immunization, and euthanized 30 days after T. cruzi challenge. Our results showed limited polarization of specific anti-ecto-NTPDase immunoglobulins in mice receiving both immunization protocols. Conversely, the Prime-boost strategy stimulated the Th1 protective phenotype, upregulating TNF-α and downregulating IL-10 production while increasing the activation/distribution of CD3+/CD8+, CD4+/CD44hi and CD8+/CD44hi/CD62L cells in immunized and infected mice. Furthermore, IL-6 and IL10 levels were reduced, while the distribution of CD4+/CD44hi and CD3+/CD8+ cells was increased from rNTPDase-1 and DNA-NTPDase1-based immunization strategies. Animals receiving DNA-NTPDase1 and Prime-boost protocols before T. cruzi challenged exhibited an enhanced immunological response associated with IL-17 upregulation and remarkable downregulation of heart parasitism (T. cruzi DNA) and mortality. These findings indicated that NTPDase-1 with Prime-boost strategy induced a protective and sustained Th17 response, enhancing host resistance against T. cruzi. Thus, ecto-NTPDase is a potentially relevant and applicable in the development of biopharmaceuticals with greater immunoprophylactic potential for Chagas disease.

Green Tea Infusion Ameliorates Histological Damages in Testis and Epididymis of Diabetic Rats.

Green tea is a popular drink used for therapeutic purposes to mitigate the consequences of diabetes. In this study, we aimed at evaluating the potential of green tea infusion to ameliorate structural and enzymatic damages caused by hyperglycemia in the testis and epididymis of Wistar rats. For that, nondiabetic and streptozotocin-induced diabetic rats (negative control and diabetes control, respectively) received 0.6 mL of water by gavage. Another set of diabetic animals received 100 mg/kg of green tea infusion diluted in 0.6 mL of water/gavage (diabetes + green tea) daily. After 42 days of treatment, the testes and epididymides were removed and processed for histopathological analysis, micromineral determination, and enzymatic assays. The results showed that treatment with green tea infusion preserved the testicular and epididymal histoarchitecture, improving the seminiferous epithelium and the sperm production previously affected by diabetes. Treatment with green tea reduced tissue damages caused by this metabolic condition. Given the severity of hyperglycemia, there was no efficacy of the green tea infusion in maintaining the testosterone levels, antioxidant enzyme activity, and microminerals content. Thus, our findings indicate a protective effect of this infusion on histological parameters, with possible use as a complementary therapy for diabetes.

Prepubertal exposure to arsenic alters male reproductive parameters in pubertal and adult rats.

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.

Reproductive disorders in female rats after prenatal exposure to sodium arsenite.

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.

Impact of Early Arsenic Exposure on the Mineral Content and Oxidative Status of the Liver and Kidney of Pubescent and Adult Rats.

This study evaluated the effect of prepubertal arsenic exposure in the liver and kidney of pubescent rats and their reversibility 30 days after arsenic withdrawal. Male pups of Wistar rats (21 days old) were divided into two groups (n = 20/group): control animals received filtered water, and exposed rats received 10 mg L-1 arsenic from postnatal day (PND) 21 to PND 51. The liver and kidney of 52 days old rats (n = 10/group) were examined to investigate the effects of arsenic on micromineral content, antioxidant enzyme activity, histology, and biochemistry parameters. The other animals were kept alive under free arsenic conditions until 82 days old and further analyzed by the same parameters. Our results revealed that 52-day-old rats increased arsenic content in their liver and arsenic and manganese in their kidney. In those animals, glycogen and zinc content and catalase activity were reduced in the liver, and the selenium content decreased in the kidney. Thirty days later, arsenic reduced the manganese and iron content and SOD and CAT activity in the liver of 82-day-old rats previously exposed to arsenic, while glycogen and selenium content decreased in their kidney. In contrast, PND 82 rats exhibited higher retention of copper in the liver, an increase in iron and copper content, and CAT and GST activity in the kidney. Significant histological alterations of liver and kidney tissues were not observed in rats of both ages. We conclude that arsenic-induced toxicity could alter differently the oxidative status and balance of trace elements in pubertal and adult rats, demonstrating that the metalloid can cause effects in adulthood.

Bioinsecticide spinosad poses multiple harmful effects on foragers of Apis mellifera.

There are multifactorial causes for the recent decline in bee populations, which has resulted in compromised pollination and reduced biodiversity. Bees are considered one of the most important non-target insects affected by insecticides used in crop production. In the present study, we investigated the effects of acute oral exposure to spinosad on the survival, food consumption, flight behavior, respiration rate, activity of detoxification enzymes, total antioxidant capacity (TAC), brain morphology, and hemocyte count of Apis mellifera foragers. We tested six different concentrations of spinosad for the first two analyses, followed by LC50 (7.7 mg L-1) for other assays. Spinosad ingestion decreased survival and food consumption. Exposure to spinosad LC50 reduced flight capacity, respiration rate, and superoxide dismutase activity. Furthermore, this concentration increased glutathione S-transferase activity and the TAC of the brain. Notably, exposure to LC50 damaged mushroom bodies, reduced the total hemocyte count and granulocyte number, and increased the number of prohemocytes. These findings imply that the neurotoxin spinosad affects various crucial functions and tissues important for bee performance and that the toxic effects are complex and detrimental to individual homeostasis.

Investigating the effects of mesotrione/atrazine-based herbicide on honey bee foragers.

A mixture of the herbicides mesotrione and atrazine (Calaris®) is a widely used herbicide in agriculture in several countries. However, the possible toxicological effects of this formulation on non-target organisms require investigation. In this study, the effects of acute oral exposure to Calaris® were evaluated in Apis mellifera foragers. The effect of seven different concentrations of Calaris® on survival and sucrose consumption was studied, while the recommended concentration for field use (FC) and its 10× dilution (0.1 FC) were used to assess overall locomotor activity, respiratory rate, flight, midgut morphology, oxidative and nitrosative stresses, and hemocyte counting. The exposure to FC or 0.1 FC decreased locomotor activity and induced damage to the midgut epithelium. Additionally, the two tested concentrations reduced superoxide dismutase activity, nitric oxide levels, and total hemocyte count. FC also increased malondialdehyde content and 0.1 FC increased respiratory rate and decreased the proportion of prohemocytes. Overall, our findings evidenced significant harmful effects on A. mellifera foragers resulting from the ingestion of the Calaris® herbicide.

Midgut Cell Damage and Oxidative Stress in Partamona helleri (Hymenoptera: Apidae) Workers Caused by the Insecticide Lambda-Cyhalothrin.

The stingless bee Partamona helleri plays a role in pollinating both native and cultivated plants in the Neotropics. However, its populations can be reduced by the pyrethroid insecticide lambda-cyhalothrin. This compound may cross the intestinal barrier and circulate through the hemolymph, affecting various non-target bee organs. The aim of the present study was to assess the extent of cellular damage in the midgut and the resulting oxidative stress caused by lambda-cyhalothrin in P. helleri workers. Bees were orally exposed to lambda-cyhalothrin. The lethal concentration at which 50% of the bees died (LC50) was 0.043 mg a.i. L-1. The P. helleri workers were fed this concentration of lambda-cyhalothrin and their midguts were evaluated. The results revealed signs of damage in the midgut epithelium, including pyknotic nuclei, cytoplasm vacuolization, changes in the striated border, and the release of cell fragments, indicating that the midgut was compromised. Furthermore, the ingestion of lambda-cyhalothrin led to an increase in the activity of the detoxification enzyme superoxide dismutase and the levels of the NO2/NO3 markers, indicating oxidative stress. Conversely, the activities of the catalase and glutathione S-transferase enzymes decreased, supporting the occurrence of oxidative stress. In conclusion, the ingestion of lambda-cyhalothrin by P. helleri workers resulted in damage to their midguts and induced oxidative stress.

Impact of copper sulfate on survival, behavior, midgut morphology, and antioxidant activity of Partamona helleri (Apidae: Meliponini).

Copper sulfate (CuSO4) is widely used in agriculture as a pesticide and foliar fertilizer. However, the possible environmental risks associated with CuSO4 use, particularly related to pollinating insects, have been poorly studied. In this study, we evaluated both lethal and sublethal effects of CuSO4 on the stingless bee Partamona helleri. Foragers were orally exposed to five concentrations of CuSO4 (5000, 1666.7, 554.2, 183.4, 58.4 µg mL-1), and the concentration killing 50% (LC50) was estimated. This concentration (142.95 µg mL-1) was subsequently used in behavioral, midgut morphology, and antioxidant activity analyses. Bee mortality increased with the ingestion of increasing concentrations of CuSO4. Ingestion at the estimated LC50 resulted in altered walking behavior and damage to the midgut epithelium and peritrophic matrix of bees. Furthermore, the LC50 increased the catalase or superoxide dismutase activities and levels of the lipid peroxidation biomarker malondialdehyde. Furthermore, the in situ detection of caspase-3 and LC3, proteins related to apoptosis and autophagy, respectively, revealed that these processes are intensified in the midgut of treated bees. These data show that the ingestion of CuSO4 can have considerable sublethal effects on the walking behavior and midgut of stingless bees, and therefore could pose potential risks to pollinators including native bees. Graphical abstract.

High Seasonal Variation of Plasma Testosterone Levels for a Tropical Grassland Bird Resembles Patterns of Temperate Birds.

AbstractTestosterone (T) is a sexual hormone capable of modulating several traits in birds, including aggressiveness and reproductive behavior. Although variation in T-related traits is well-known for temperate zone birds, this variation has not been extensively studied in tropical species. The campo miner (Geositta poeciloptera) is a threatened bird endemic to the grasslands of the South American Cerrado. We investigated the seasonal variation in plasma T levels and associated behavior in the campo miner, addressing the following questions: (1) Does the species exhibit seasonal variation in T profile? (2) Do males have higher plasma T levels than females, irrespective of season? (3) Are males with higher plasma T levels more aggressive than males with lower T levels? (4) Do males' plasma T levels decrease after females lay eggs? We found that T levels are higher during the breeding season than during the nonbreeding season and that males present higher T levels than females throughout the year. Such high T levels are associated with a higher probability to engage in aggressive behavior; however, T levels decline toward the egg-laying date and keep decreasing afterward. Higher T levels before egg laying are apparently related to territorial defense against invaders and extrapair copulations. With the beginning of parental care, T levels decrease, which is in line with previous observations that the species becomes less aggressive after egg laying. This study contributes to the understanding of environmental endocrinology of tropical birds, filling some knowledge gaps about the diverse Neotropical avifauna.

Acute exposure to fipronil induces oxidative stress, apoptosis and impairs epithelial homeostasis in the midgut of the stingless bee Partamona helleri Friese (Hymenoptera: Apidae).

Partamona helleri is an important pollinator in natural and agricultural ecosystems in the neotropics. However, the foraging activity of this bee increases its risk of exposure to pesticides, which may affect both the individuals and the colony. Thus, this study aims to evaluate the side effects of LC50 of fipronil (0.28 ng a.i. µL-1) on the midgut morphology, antioxidant activity and some pathways of cell death, proliferation and differentiation in workers of P. helleri, after 24 h of oral exposure. Fipronil caused morphological alterations in the midgut of the bees. The activities of the detoxification enzymes superoxide dismutase, catalase and glutathione S-transferase increased after exposure, which suggests the occurrence of a detoxification mechanism. Furthermore, exposure to fipronil changed the number of positive cells for signaling-pathway proteins in the midgut of bees, which indicates the induction of cell death by the apoptotic pathway and impairment of the midgut epithelial regeneration. These results demonstrate that fipronil may negatively affect the morphology and physiology of the midgut of the stingless bee P. helleri and impose a threat to the survival of non-target organisms.

Harmful effects of fipronil exposure on the behavior and brain of the stingless bee Partamona helleri Friese (Hymenoptera: Meliponini).

Fipronil is a pesticide widely used to control agricultural and household insect pests. However, fipronil is highly toxic to non-target insects, including pollinators. In this study, we investigated the acute effects of fipronil on the behavior, brain morphology, antioxidant activity, and proteins related to signaling pathways on the brain of workers of the stingless bee Partamona helleri. The ingestion of fipronil increases both the walking distance and velocity and causes enlarged intercellular spaces in the Kenyon cells and intense vacuolization in the neuropils of the brain. Moreover, fipronil decreases the activity of catalase (CAT) and increases the activity of glutathione S-transferase (GST). However, there is no difference in superoxide dismutase (SOD) activity between the control and fipronil. Regarding immunofluorescence analysis, bees exposed to fipronil showed an increase in the number of cells positive for cleaved caspase-3 and peroxidase, but a reduction in the number of cells positive for ERK 1/2, JNK and Notch, suggesting neuron death and impaired brain function. Our results demonstrate that fipronil has harmful effects on the behavior and brain of a stingless bee, which may threaten the individuals and colonies of this pollinator.

High-fat diet and caffeine interact to modulate bone microstructure and biomechanics in mice.

AIMS: Although excessive fat and caffeine intake are independent risk factors for bone microstructural and functional disturbances, their association remains overlooked. Thus, we investigated the impact of high-fat diet (HFD) and caffeine alone and combined on serum lipid profile, bone microstructure, micromineral distribution and biomechanical properties. METHODS: Forty female C57BL/6 mice were randomized into 4 groups daily treated for seventeen weeks with standard diet (SD) or HFD (cafeteria diet) alone or combined with 50 mg/kg caffeine. KEY FINDINGS: The association between HFD and caffeine reduced the weight gain compared to animals receiving HFD alone. Caffeine alone or combined with HFD increases total and HDL cholesterol circulating levels. HFD also reduced calcium, phosphorus and magnesium bone levels compared to the groups receiving SD, and this reduction was aggravated by caffeine coadministration. From biomechanical assays, HFD combined with caffeine increased bending strength and stiffness of tibia, a finding aligned with the marked microstructural remodeling of the cortical and cancellous bone in animals receiving this combination. SIGNIFICANCE: Our findings indicated that HFD and caffeine interact to induce metabolic changes and bone microstructural remodeling, which are potentially related to bone biomechanical adaptations in response to HFD and caffeine coadministration.

Impact of prenatal arsenic exposure on the testes and epididymides of prepubertal rats.

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.

Arsenic induces dose-dependent structural and ultrastructural pathological remodeling in the heart of Wistar rats.

AIM: Arsenic, an environmental contaminant, represents a public health problem worldwide. Studies have shown its association with molecular mechanisms related to cardiomyocytes redox balance. However, the microstructure and ultrastructure of cardiac tissue, as well as the activity of its antioxidant defenses front of disturbances in the mineral bioavailability induced by arsenic are still scarce. Thus, the aim of this study was to evaluate if arsenic exposure might induce structural and ultrastructural damages in cardiac tissue, including pathological remodeling of the parenchyma and stroma. Moreover, its impact on micromineral distribution and antioxidant enzymes activity in heart tissue was also evaluated. MAIN METHODS: Adult male Wistar rats were divided into three groups that received 0, 1 and 10 mg/L sodium arsenite in drinking water for eight weeks. The hearts were collected and subjected to structural and ultrastructural analysis, mineral microanalysis and antioxidant enzymes quantification. Functional markers of cardiac damages were evaluated using serum samples. KEY FINDINGS: Arsenic exposure induced dose-dependent structural and ultrastructural remodeling of cardiac tissue, with parenchyma loss, increase of stroma components, collagen deposition, and pathological damages such as inflammation, sarcomere disorganization, mitochondria degeneration and myofilament dissociation. Moreover, this metalloid was bioaccumulated in the tissue affecting its micromineral content, which resulted in antioxidant imbalance and increased levels of oxidative stress and cardiac markers. SIGNIFICANCE: Taken together, our findings indicate that the heart is a potential target to arsenic toxicity, and long-term exposure to this metalloid must be avoided, once it might induce several cardiac tissue pathologies.

Lipophosphoglycan-3 recombinant protein vaccine controls hepatic parasitism and prevents tissue damage in mice infected by Leishmania infantum chagasi.

AIMS: 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. MAIN METHODS: 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. KEY FINDINGS: 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. SIGNIFICANCE: 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.

Arsenic exposure intensifies glycogen nephrosis in diabetic rats.

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.

Reproductive functions in Desmodus rotundus: A comparison between seasons in a morphological context.

Reproductive seasonality in Neotropical bats has been assessed to the better understand their reproductive behavior. This knowledge is especially important for the control of Desmodus rotundus population as it is a transmitter of rabies virus. Therefore, we aimed to evaluate the functional activity of testis and epididymis of D. rotundus in dry and rainy seasons under a morphological approach. We observed an increase in tubular diameter and epithelial height of the seminiferous tubules during the rainy season. In the latter, additionally, stereological analysis of the testis showed increased proportion of seminiferous epithelium and reduced percentage of lumen. The sperm number in caput/corpus epididymis increased in rainy season, whereas sperm count and transit time were reduced in cauda region. These alterations were probably related to the recovery of epithelium activities after mating season in dry season. Despite altered nuclear and cytoplasm parameters of Leydig cells between seasons, the volume and number of these cells were constant. Moreover, no change in serum testosterone levels, daily sperm production, and apoptotic index were observed, which indicates that the reproductive pattern in D. rotundus does not change between seasons. Our study offers a baseline for the management of vampire bat population as an attempt to control rabies disease.