Acrylamide (AA) is one of the most common toxins in foods. Its
effect on bone microstructure has not been investigated. The aim
of our study was to analyze the impact of acute exposure to AA on
femoral bone microstructure in mice. Adult animals were treated
perorally with 2 doses of AA (E1 group, 1 mg/kg b.w.) in a 24-h
period and with 3 doses of AA (E2 group, 1 mg/kg b.w.) in a 48-h
period. Mice exposed to AA had smaller sizes of primary osteon's
vascular canals. Secondary osteons were significantly smaller in
mice from E2 group; however their increased number (from 38 %
to 77 %) was identified in both E1 and E2 groups. In these groups,
a higher number of resorption lacunae (from 100 % to 122 %) was
also found. The values for bone volume, trabecular number were
increased and that for trabecular separation was decreased in mice
administered AA. Significantly higher value of bone surface was
observed in mice from E1 group whereas trabecular thickness was
increased in E2 group. The effect of AA on microstructure of
compact and trabecular bone tissues is different. In our study, one
dose of AA was used and acute effects of AA were investigated.
Therefore, further studies are needed to study mechanisms by
which AA acts on bone.
Acrylamide (AA) is a highly reactive organic compound capable of polymerization to form polyacrylamide, which is commonly used throughout a variety of industries. Given its toxic effect on humans and animals, the last 20 years have seen an increased interest in research devoted to the AA. One of the main sources of AA is food. AA appears in heated food following the reaction between amino acids and reduced sugars. Large concentrations of AA can be found in popular staples such as coffee, bread or potato products. An average daily consumption of AA is between 0.3-2.0 μg/kg b.w. Inhalation of acrylamide is related with occupational exposure. AA delivered with food is metabolized in the liver by cytochrome P450. AA biotransformation and elimination result in formation of toxic glycidamide (GA). Both, AA and GA can be involved in the coupling reaction with the reduced glutathione (GSH) forming glutathione conjugates which are excreted with urine. Biotransformation of AA leads to the disturbance in the redox balance. Numerous research proved that AA and GA have significant influence on physiological functions including signal propagation in peripheral nerves, enzymatic and hormonal regulation, functions of muscles, reproduction etc. In addition AA and GA show neurotoxic, genotoxic and cancerogenic properties. In 1994, International Agency for Research on Cancer (IARC) classified acrylamide as a potentially carcinogenic substance to human., M. Semla, Z. Goc, M. Martiniaková, R. Omelka, G. Formicki., and Obsahuje bibliografii
This study aimed at investigating the protective role of CoQ10
against cadmium (Cd)-induced reproductive toxicity in male rats.
Adult male Wistar rats were exposed to an acute dose of Cd
(25 mg/kg bwt; Cd group), Cd+CoQ10 (25 mg/kg bwt Cd+10 mg
CoQ10; Cd-Q10 group) and distilled water (control) in vivo for
15 consecutive days and semen quality was assessed.
A significant reduction was noted in sperm concentration,
progressive motility, morphology and DNA integrity in both Cdand Cd-Q10 groups in comparison to control indicating
Cd-induced testicular lipid per oxidation (LPO) and decline in
indigenous antioxidant defense system as measured by total
antioxidant capacity (TAC) (p<0.05). However, simultaneous
co-administration of CoQ10 along with Cd (Cd-Q10 group) was
able to improve sperm concentration, motility, progressive
motility, morphology, DNA integrity, and testicular TAC as well as
lower LPO compared to Cd group (p<0.05). Results indicate that
used dose of CoQ10 is capable of moderately ameliorating
reproductive toxicity of Cd by improving semen quality and
reducing testicular oxidative stress.