Publication: Cytotoxic effect of Ochratoxin A on the renal corpuscles
of rat kidney: could Ochratoxin A cause kidney failure?
Authors
Abdu, Suzan ; Ali, Awatif ; Ansari, Shatha
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Publisher
Murcia: F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
To demonstrate that Ochratoxin A can cause
kidney failure as the kidney is the primary target for
OTA cytotoxicity. Ochratoxin A (OTA) is a mycotoxin
found in our food. The cytotoxic effect of a low
cumulative dose of OTA on the renal corpuscles of the
kidney tissue has been investigated in this report. This
study was based on two groups in which weaning albino
rats were used: (1) control; (2) OTA-treated rats (289
µg/kg/day). After 28 days of treatment, a significant
decrease in body weight, kidney weight and relative
weight were detected in OTA treated rats. Serum
creatinine and urea level were slightly elevated. These
results revealed significant histological as well as
ultrastructral lesions in the OTA treated group. The
lesions included global congestion in the renal tissue and
loss of demarcation between the cortex and medulla. The
normal architecture of the renal corpuscles was
destroyed and most of the corpuscles lost their ordinary
look. The most apparent histopathological changes were
urinary space disappearance and hypercellularity. In
addition, congested, undifferentiated, atrophied,
hypertrophied, fragmented, sclerotic, degenerated, and
obliterated renal corpuscles were distinct. The
ultrastructural lesions observed in the renal corpuscles in
OTA on treated rats included; proliferation and swelling
of the endothelial cells with occasional loss of fenestrae;
narrowing of the capillary lumen; damaged podocytes
with deteriorated secondary foot processes,
hypertrophied and proliferated mesangial cells with
expanded mesangial matrix. The endothelium was
clearly defected and vacuolated, and lost its fenestrations
in many glomerular capillaries. In addition, the
glomerular basement membrane (GBM) became visibly
thickened and tortuous. Necrotic glomerular cells were
frequently observed. Pre-apoptotic cells were also seen.
It was concluded that the exposure to relatively low
OTA concentrations induced significant lesions to the
renal corpuscles. Moreover, it activated oxidative damage and necrosis which can cause extensive damage
to the kidney and ultimately kidney failure.
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