Alkaline phosphatase activity in plasma and liver of rats submitted to chronic exposure to fluoride

Fernandes, Marcelo; Iano, Flávia Godoy; Rocia, Vivian; Yanai, Marcela Mitsuko; Leite, Aline de Lima; Furlani, Tatiana Almeida; Buzalaf, Marília Afonso Rabelo; Oliveira, Rodrigo Cardoso de

doi:10.1590/s1516-89132011000600014

Cited by 10 publications

(4 citation statements)

References 22 publications

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“…The serum elevation of alanine aminotransferase (ALT) signalizes the cell membrane injury while aspartate aminotransferase (AST) refers to mitochondrial damage of hepatic tissue [ 47 ]. In addition, alkaline phosphatase (ALP) is used as an indicator of hepatobiliary disease and hepatic cellular damage [ 48 ]. In our study, an increased level of these enzymes was demonstrated which indicated hepatocyte damages mediated by the C. parvum infection in mice.…”

Section: Discussionmentioning

confidence: 99%

S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

et al. 2020

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Cryptosporidiosis has been proposed to be one of the major causes of diarrhoeal disease in humans worldwide that possesses zoonotic concern. Thereby, this study investigated the potential effects of s-Methylcysteine (SMC) on the parasite in vivo followed by the measurement of cytokines, oxidative stress parameters, and an investigation of the major histopathological changes. Sixty male Swiss albino mice weighing 20–25 g were allocated equally into five groups and orally administered saline only (control), SMC only (SMC50) (50 mg/kg b.w.), and 104Cryptosporidium parvum oocysts per mouse via an esophageal tube (C + ve untreated). The fourth and fifth groups (C + SMC25, C + SMC50) administrated 104C. parvum oocysts combined with SMC25 (low dose) and 50 (high dose) mg/kg b.w., respectively. At days 7 and 14 post-infection (PI), the feces was collected from each group in order to count C. parvum oocysts. After two weeks of treatment, the animals were euthanized and the serum was collected for biochemical analysis. Next, the intestinal, spleen, and liver sections were dissected for histopathological examination. The results revealed lower oocyst numbers in the C + SMC25 and C + SMC50 groups compared to the infected untreated group. Moreover, higher doses of SMC treatment significantly reduced the enteritis induced by C. parvum in a dose-dependent manner. The hepatic lesions were also mitigated as demonstrated in C + SMC25 and C + SMC50 groups unlike the infected group via lowering the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes and increasing albumin and globulin serum levels. SMC administration also reduced cytokines production (SAP, TNF-α, IL-6, and IFN-γ) mediated by Cryptosporidium infection in contrast to the infected untreated group. There were marked lymphoid depletion and amyloidosis observed in the infected untreated group, while the treated groups showed obvious increase in the lymphoid elements. Moreover, the scoring of intestinal parasites, hepatic, and splenic lesions in the SMC-treated groups exhibited significantly lower pathological lesions in different organs in a dose-dependent manner, compared to the infected untreated group. Our results also revealed a significant change in the malondialdehyde content with an elevation of glutathione and superoxide dismutase in the intestines collected from C + SMC25 and C + SMC50 mice relative to the untreated group. Taken together, our results indicated that SMC could be a promising effective compound for treating and declining C. parvum infestation via restoring structural alterations in different tissues, enhancing antioxidant enzymes, and suppressing the cytokines liberation.

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Section: Discussionmentioning

confidence: 99%

S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

et al. 2020

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“…A previous study has shown that an elevated level of AST in serum indicates damage to the mitochondria of the liver tissue (36). Moreover, elevated levels of ALP and ALT are used as signs of hepatic cellular damage and hepatobiliary diseases (37). In the present study, elevated levels of the enzymes AST, ALT, and ALP in the Inf.Unt mouse group indicated that C. parvum causes damage to hepatocyte in juvenile mice.…”

Section: Unt G R O U P C O M P a R E D W I T H O T H E R G R O U P S ...mentioning

confidence: 56%

Chitosan Protects Immunosuppressed Mice Against Cryptosporidium parvum Infection Through TLR4/STAT1 Signaling Pathways and Gut Microbiota Modulation

Rahman

Gong

et al. 2022

Front. Immunol.

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Cryptosporidium parvum infection is very common in infants, immunocompromised patients, or in young ruminants, and chitosan supplementation exhibits beneficial effects against the infection caused by C. parvum. This study investigated whether chitosan supplementation modulates the gut microbiota and mediates the TLR4/STAT1 signaling pathways and related cytokines to attenuate C. parvum infection in immunosuppressed mice. Immunosuppressed C57BL/6 mice were divided into five treatment groups. The unchallenged mice received a basal diet (control), and three groups of mice challenged with 1 × 106 C. parvum received a basal diet, a diet supplemented with 50 mg/kg/day paromomycin, and 1 mg/kg/day chitosan, and unchallenged mice treated with 1 mg/kg/day chitosan. Chitosan supplementation regulated serum biochemical indices and significantly (p < 0.01) reduced C. parvum oocyst excretion in infected mice treated with chitosan compared with the infected mice that received no treatment. Chitosan-fed infected mice showed significantly (p < 0.01) decreased mRNA expression levels of interferon-gamma (IFN-γ) and tumor necrosis factor-α (TNF-α) compared to infected mice that received no treatment. Chitosan significantly inhibited TLR4 and upregulated STAT1 protein expression (p < 0.01) in C. parvum-infected mice. 16S rRNA sequencing analysis revealed that chitosan supplementation increased the relative abundance of Bacteroidetes/Bacteroides, while that of Proteobacteria, Tenericutes, Defferribacteres, and Firmicutes decreased (p < 0.05). Overall, the findings revealed that chitosan supplementation can ameliorate C. parvum infection by remodeling the composition of the gut microbiota of mice, leading to mediated STAT1/TLR4 up- and downregulation and decreased production of IFN-γ and TNF-α, and these changes resulted in better resolution and control of C. parvum infection.

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“…AP activity in blood plasma was increased in K33 males, which may be related to the high fluorine content of the krill. Serum AP has been reported to be elevated in rats given 50 ppm fluoride in drinking water for 60 days, 45 and mink fed diets containing 194 ppm supplemental fluorine (from NaF). 40 Increased AP activity is associated with increased osteoblast activity 46 liver injury.…”

Section: Blood Characteristicsmentioning

confidence: 99%

Antarctic krill meal as an alternative protein source in pet foods evaluated in mink (Neovison vison). II. Growth

Krogdahl¹,

Ahlstrøm²,

Burri³

et al. 2015

OAAP

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Background: Antarctic krill meal has potential for use in pet food as a source of protein and lipids. An experiment was conducted in growing male and female mink to evaluate the safety of Antarctic krill meal as an ingredient for pet food. Materials and methods: In the first growth period, the levels of krill were 0%, 8%, 17%, and 33% of dry matter. The levels were slightly less in the second growth period (0%, 8%, 16%, and 32% of dry matter). The four diets used were labeled K0, K8, K17, and K33 for both growth periods. The experiments included assessments of growth, hematology, clinical chemistry, tissue histology, liver and kidney mineral concentrations, and bone fluoride accumulation. Results: Mink receiving Antarctic krill meal grew at the same rate as controls, suggesting that protein and energy values of the krill meal were comparable to the control fishmeal. Relative organ weights of animals were the same for the K0, K8, and K17 groups, whereas K33 animals showed higher values for weights of the stomach and rectum. Hematological, clinical chemistry, and morphological analyses did not differ between animals fed K0 and K8 diets. Animals in the K17 and K33 groups showed some histological changes in the liver and kidney, and a few alterations in some clinical chemistry and hematology values related to nutrient intake or metabolism. Joint/bone deformities were observed in K33 mink. Conclusion: Antarctic krill meal has a similar nutritional value as good-quality fishmeal and produces no adverse effects in growing mink at levels up to 8% of dry matter. The results suggest that Antarctic krill meal can be safely included in pet food for growing animals.

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Alkaline phosphatase activity in plasma and liver of rats submitted to chronic exposure to fluoride

Cited by 10 publications

References 22 publications

S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

Chitosan Protects Immunosuppressed Mice Against Cryptosporidium parvum Infection Through TLR4/STAT1 Signaling Pathways and Gut Microbiota Modulation

Antarctic krill meal as an alternative protein source in pet foods evaluated in mink (Neovison vison). II. Growth

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