Influence of chronic Cd intoxification on the alkaline phosphatase activity of liver and kidney; biochemical, histochemical and histological investigations

Peereboom-Stegeman, J.H.J. Copius; Melet, J; Peereboom, J. W. Copius; Hooghwinkel, G. J. M.

doi:10.1016/0300-483x(79)90092-1

Cited by 22 publications

(3 citation statements)

References 12 publications

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“…A decrease in ALP levels is directly related to atrophy of the seminiferous tubules, a decrease in the mature sperm count in the tubules, shedding of seminiferous epithelium, and morphological abnormalities of Sertoli cells [ 50 ]. In our study, the activity of the testicular marker enzyme ALP decreased, which matched the results reported in other studies [ 51 ]. Similarly, the activity of ACP increased, which also matched the results reported in other studies [ 52 , 53 ].…”

Section: Discussionsupporting

confidence: 93%

Anthocyanins from Lycium ruthenicum Murray Mitigate Cadmium-Induced Oxidative Stress and Testicular Toxicity by Activating the Keap1/Nrf2 Signaling Pathway

Dong,

Lu,

Xue

et al. 2024

Pharmaceuticals

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Cadmium (Cd) is a hazardous heavy metal environmental pollutant that has carcinogenic, teratogenic, and mutagenic properties. Excessive exposure to Cd can induce oxidative stress, which greatly harms the male reproductive system. Anthocyanins have remarkable antioxidative, anti-inflammatory, and anti-stress properties. In this study, we investigated the effects of anthocyanins and the underlying mechanisms through which anthocyanins mitigate Cd-induced reproductive damage. We isolated and purified Lycium ruthenicum Murray anthocyanin extract (LAE) and performed UHPLC-MS/MS to identify 30 different anthocyanins. We established an ICR mouse Cd injury model by administering 5 mg/kg/day CdCl2 for 28 consecutive days. LAE at 500 mg/kg/day effectively ameliorated testicular damage and preserved spermatogenesis. The mice in the LAE-treated group had elevated testosterone and inhibin B levels. Additionally, the treatment restored the activity of antioxidant enzymes, including T-SOD, CAT, and GR, and substantially increased the levels of the non-enzymatic antioxidant GSH. Research findings indicate that LAE can activate the SIRT1/Nrf2/Keap1 antioxidant pathway. This activation is achieved through the upregulation of both the SIRT1 gene and protein levels, leading to the deacetylation of Nrf2. Moreover, LAE reduces the expression of Keap1, alleviating its inhibitory effect on Nrf2. This, in turn, facilitates the uncoupling process, promoting the translocation of Nrf2 to the nucleus, where it governs downstream expression, including that of HO-1 and GPX1. LAE effectively mitigated toxicity to the reproductive system associated with exposure to the heavy metal Cd by alleviating oxidative stress in the testes.

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Section: Discussionsupporting

confidence: 93%

Anthocyanins from Lycium ruthenicum Murray Mitigate Cadmium-Induced Oxidative Stress and Testicular Toxicity by Activating the Keap1/Nrf2 Signaling Pathway

Dong,

Lu,

Xue

et al. 2024

Pharmaceuticals

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“…In considering the implications of the present findings, it is important to note that the Cd dose and treatment protocol that were employed in these studies are similar to those that have been used by many other investigators (Aoyagi et al, 2003; Dudley et al, 1985; Goyer et al, 1989; Peereboom-Stegeman et al, 1979; Shaikh et al, 1999; Suzuki, 1980; Tanimoto et al, 1993). This Cd treatment regimen results in consistent changes in a wide variety of parameters including: body weight, urine volume, urinary protein excretion and renal Cd levels.…”

Section: Discussionmentioning

confidence: 75%

“…High levels of Cd are clearly capable of causing proximal tubule necrosis (Brzoska et al, 2003; Dudley et al, 1985; Goyer et al, 1989; Kjellstrom, 1986; Sudo et al, 1996; Peereboom-Stegeman et al, 1979). However, other studies indicate that the early stages of Cd nephrotoxicity primarily involve apoptosis of proximal tubule epithelial cells, with little evidence of necrosis (Aoyagi et al, 2003; Hamada et al, 1991; Tanimoto et al, 1993; Yan et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Expression of kidney injury molecule-1 (Kim-1) in relation to necrosis and apoptosis during the early stages of Cd-induced proximal tubule injury

Prozialeck

Edwards

Lamar

et al. 2009

Toxicology and Applied Pharmacology

113

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Cadmium (Cd) is a nephrotoxic industrial and environmental pollutant that causes a generalized dysfunction of the proximal tubule. Kim-1 is a transmembrane glycoprotein that is normally not detectable in non-injured kidney, but is up-regulated and shed into the urine during the early stages of Cd-induced proximal tubule injury. The objective of the present study was to examine the relationship between the Cd-induced increase in Kim-1 expression and the onset of necrotic and apoptotic cell death in the proximal tubule. Adult male Sprague-Dawley rats were treated with 0.6 mg (5.36 μmoles) Cd/kg, subcutaneously, 5 days per week for up to 12 weeks. Urine samples were analyzed for levels of Kim-1 and the enzymatic markers of cell death, lactate dehydrogenase (LDH) and alpha-glutathione-S-transferase (α-GST). In addition, necrotic cells were specifically labeled by perfusing the kidneys in situ with ethidium homodimer using a procedure that has been recently developed and validated in the Prozialeck laboratory. Cryosections of the kidneys were also processed for the immunofluorescent visualization of Kim-1 and the identification of apoptotic cells by TUNEL labeling. Results showed that significant levels of Kim-1 began to appear in the urine after 6 weeks of Cd treatment, whereas the levels of total protein, α-GST and LDH were not increased until 8-12 weeks. Results of immunofluorescence labeling studies showed that after 6 weeks and 12 weeks, Kim-1 was expressed in the epithelial cells of the proximal tubule, but that there was no increase in the number of necrotic cells, and only a modest increase in the number of apoptotic cells at 12 weeks. These results indicate that the Cd-induced increase in Kim-1 expression occurs before the onset of necrosis and at a point where there is only a modest level of apoptosis in the proximal tubule.

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Acid and alkaline phosphatase activities in the clam Ruditapes philippinarum

1993

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Influence of chronic Cd intoxification on the alkaline phosphatase activity of liver and kidney; biochemical, histochemical and histological investigations

Cited by 22 publications

References 12 publications

Anthocyanins from Lycium ruthenicum Murray Mitigate Cadmium-Induced Oxidative Stress and Testicular Toxicity by Activating the Keap1/Nrf2 Signaling Pathway

Anthocyanins from Lycium ruthenicum Murray Mitigate Cadmium-Induced Oxidative Stress and Testicular Toxicity by Activating the Keap1/Nrf2 Signaling Pathway

Expression of kidney injury molecule-1 (Kim-1) in relation to necrosis and apoptosis during the early stages of Cd-induced proximal tubule injury

Acid and alkaline phosphatase activities in the clam Ruditapes philippinarum

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