26 research outputs found
Effects of clothianidin exposure on sperm quality, testicular apoptosis and fatty acid composition in developing male rats
Clothianidin (CTD) is one of the latest members
of the synthetic organic insecticides, the neonicotinoids.
In the present study, it was aimed to investigate if
daily oral administration of CTD at low doses for
90 days has any deleterious effects on reproductive
functions of developing male rats. Animals were randomly
divided into four groups of six rats each, assigned
as control rats, or rats treated with 2 (CTD-2), 8 (CTD-8)
or 32 (CTD-32) mg CTD/kg body weight by oral gavage.
The significant decreases of the absolute weights
of right cauda epididymis and seminal vesicles, and
body weight were detected in the animals exposed to
CTD administration at 32 mg/kgBW/day. Epididymal
sperm concentration decreased significantly in CTD-32
group and the abnormal sperm rates increased in CTD-
8 and CTD-32 groups when compared to control group.
The testosterone level was significantly decreased in
CTD-32 group when compared to control group. The
administration of all CTD doses resulted in a significant
decrease in the level of GSH. The number of TUNELpositive
cells significantly increased in the germinal
epithelium of testis of rats exposed to CTD at
32 mg/kgBW/day. In groups CTD-8 and CTD-32,
only docosapentaenoic, arachidonic, palmitic and palmitoleic
acids were significantly elevated when compared
to control. The ratios of 20:4/18:2 and 18:1n−9/
18:0 were decreased when rats exposed to CTD. Sperm
DNA fragmentation was observed in CTD-32 group,
but not CTD-2 and CTD-8. It is concluded that low
doses of CTD exposure during critical stages of sexual maturation had moderate detrimental effects on reproductive
organ system and more severe effects are likely
to be observed at higher dose levels. In addition, the
reproductive system may be more sensitive to exposure
of CTD even earlier in development (prenatal and early
postnatal), and therefore it could be expected that more
severe effects could also be observed at the NOAEL
dose levels, if dosing had occurred in utero or early
postnatal
Insecticide imidacloprid induces morphological and DNA damage through oxidative toxicity on the reproductive organs of developing male rats
We investigated whether treatment with imidacloprid would induce morphological changes, DNA fragmentation, antioxidant imbalance
and apoptosis in the reproductive system of developing male rats. Twenty-four male rats were included in this 90-day study, starting at 7 days of
age. The rats were divided into four groups. The first group was used as control. The second, third and fourth groups received oral 0.5-, 2- and
8-mg/kg imidacloprid, respectively. Serum, spermand testis sampleswere collected fromall groups at the end of the experimental period. Theweights
of the epididymis, vesicula seminalis, epididymal sperm concentration, body weight gain, testosterone and reduced glutathione values were lower in
the imidacloprid-treated groups than that in the controls. All treated groups had increased lipid peroxidation, fatty acid concentrations and higher rates
of abnormal sperm. Apoptosis and fragmentation of seminal DNA were higher in rats treated at the two higher doses of imidacloprid. These results
show that this compound has a negative effect on sperm and testis of rat
Protective effects of nanostructures of hydrated C60 fullerene on reproductive function in streptozotocin-diabetic male rats
Diabetes mellitus is a well-recognized cause of male sexual dysfunction and impairments of male fertility.
Streptozotocin (STZ) is used for medical treatment of neoplastic islet -cells of pancreas and producing of
animal model of diabetes mellitus type 1 that is characterized by suppression of reproductive activity due
to the hyperglycaemia-induced oxidative stress and histopathological alterations in testes. Seeking for
the agents that could alleviate diabetes-induced damage to reproductive system is yet the important area
of inquiry. The present study was designed to evaluate whether hydrated C60 fullerene (C60HyFn), which
is known to be powerful bioantioxidant, eliminate testicular dysfunction induced by STZ-diabetes in rats.
Wistar strain male albino rats were divided into four groups of six animals each: (1) control group, (2)
C60HyFn-treated nondiabetic group, (3) STZ-diabetic group and (4) C60HyFn-treated diabetic group. Once
hyperglycaemia was induced by STZ, rats in the second and fourth groups were treated with C60HyFn (in
the form of drinking water) at the dose of 4 g/kg daily for 5 weeks. In diabetic rats, relative weights of
right cauda epididymis, seminal vesicles, prostate, sperm motility and epididymal sperm concentration
were significantly less than those of control group, but which were restored in the fourth group treated
with C60HyFn (p < 0.001). In hematoxylin and eosin staining, marked histopathological changes including
degeneration, desquamation, disorganisation and reduction in germinal cells, interstitial oedema and
congestion were evident in the testis of diabetic rats, but C60HyFn treatment resulted in recovery of
histopathological changes and an increase in Johnsen’s testicular score significantly (p < 0.001). C60HyFn
treatment restores the increased apoptosis induced by STZ-diabetes. In diabetic rats, levels of serum
testosterone, testicular reduced glutathione (GSH) and alpha-tocopherol were significantly reduced and
testicular lipid peroxidation level was increased (p < 0.001). Nevertheless, treatment of diabetic rats with
C60HyFn resulted in significant corrective effects on these parameters towards the control levels. C60HyFn,
applied alone, did not exert any toxic effects in testicular tissues. Furthermore, C60HyFn treatment in
diabetic and nondiabetic rats resulted in considerable elevations of some important polyunsaturated
fatty acids. In conclusion, we have presented for the first time substantial evidence that administration
of C60HyFn significantly reduces diabetes-induced oxidative stress and associated complications such as
testicular dysfunction and spermatogenic disruptio
Comparative analysis of the protective effects of melatonin and vitamin E on streptozocin-induced diabetes mellitus
There is a clearly documented link between diabetic complications and lipid peroxidation. Hyperglycemia causes a reduction in levels of protective endogenous antioxidants and increases generation of free radicals. The present Study was carried out to compare the protective effects of melatonin and vitamin E against streptozocin (STZ)-induced diabetes in rats. Melatonin was administered s.c. (100 mug/kg) whereas vitamin E was given i.p. (100 mg/kg) after induction of diabetes with STZ (60 mg/kg). Plasma total cholesterol, triglyceride and low density lipoprotein (LDL) levels were increased in STZ group while both melatonin and vitamin E injection caused a significant decrease in the levels of all these parameters. The lipid lowering effect of melatonin was greater than that of vitamin E. Melatonin caused a significant decrease in brain, liver and kidney tissue malondialdehyde (MDA) levels which were increased because of STZ-induced diabetes. Vitamin E also reduced elevated NIDA concentrations in diabetic rat tissues, but the effect of melatonin vas more potent than that of vitamin E. Furthermore, treatment of diabetic rats with melatonin increased brain and kidney glutathione peroxidase (GSH-Px) activity to the levels below that of control rats. Vitamin E was found to be less effective on GSH-Px activity levels in brain and kidney than melatonin whereas it was more potent than melatonin in liver. In summary, melatonin prevents many diabetic complications by reducing oxidative stress and protects organisms from oxidative damage and dyslipidemia. Considering the much lower molar concentration of melatonin compared with vitamin E, melatonin seems to be a more potent antioxidant, especially in the brain and kidney. There is a clearly documented link between diabetic complications and lipid peroxidation. Hyperglycemia causes a reduction in levels of protective endogenous antioxidants and increases generation of free radicals. The present study was carried out to compare the protective effects of melatonin and vitamin E against streptozocin (STZ)-induced diabetes in rats. Melatonin was administered s.c. (100 microg/kg) whereas vitamin E was given i.p. (100 mg/kg) after induction of diabetes with STZ (60 mg/kg). Plasma total cholesterol, triglyceride and low density lipoprotein (LDL) levels were increased in STZ group while both melatonin and vitamin E injection caused a significant decrease in the levels of all these parameters. The lipid lowering effect of melatonin was greater than that of vitamin E. Melatonin caused a significant decrease in brain, liver and kidney tissue malondialdehyde (MDA) levels which were increased because of STZ-induced diabetes. Vitamin E also reduced elevated MDA concentrations in diabetic rat tissues, but the effect of melatonin was more potent than that of vitamin E. Furthermore, treatment of diabetic rats with melatonin increased brain and kidney glutathione peroxidase (GSH-Px) activity to the levels below that of control rats. Vitamin E was found to be less effective on GSH-Px activity levels in brain and kidney than melatonin whereas it was more potent than melatonin in liver. In summary, melatonin prevents many diabetic complications by reducing oxidative stress and protects organisms from oxidative damage and dyslipidemia. Considering the much lower molar concentration of melatonin compared with vitamin E, melatonin seems to be a more potent antioxidant, especially in the brain and kidney.</p
Lack of antioxidant hormone melatonin causes increase in homocysteine levels in pinealectomized rats
Effect of melatonin on oxidative status of rat brain, liver and kidney tissues under constant light exposure
An enormous amount of data has been published in recent years demonstrating melatonin's defensive role against toxic free radicals. In the present study, we examined the role of melatonin as an antioxidant against the effect of continuous light exposure. Rats were divided into three groups. Control rats (group A) were kept under natural conditions whereas other group of rats (group B and C) were exposed to constant light for inhibition of melatonin secretion by the pineal gland. Group C rats also received melatonin via s.c. injection (1 mg kg(-1) body weight day(-1)). At the end of experiment, ail animals were sacrificied by decapitation, serum and tissue samples were removed for determination of malondialdehyde (MDA), a product of lipid peroxidation, conjugated dienes levels and glutathione peroxidase (GSH-Px) activity levels. It was found that lipid peroxidation was increased in the rats which were exposed to constant light. Melatonin injection caused a decrease in lipid peroxidation, especially in the brain. In addition, melatonin application resulted in increased GSH-Px activity, which has an antioxidant effect. Thus, melatonin is not only a direct scavenger of toxic radicals, but also stimulates the antioxidative enzyme GSH-Px activity to detoxify hydroxyl radical produced by constant light exposure. Copyright (C) 2001 John Wiley & Sons, Ltd.An enormous amount of data has been published in recent years demonstrating melatonin's defensive role against toxic free radicals. In the present study, we examined the role of melatonin as an antioxidant against the effect of continuous light exposure. Rats were divided into three groups. Control rats (group A) were kept under natural conditions whereas other group of rats (group B and C) were exposed to constant light for inhibition of melatonin secretion by the pineal gland. Group C rats also received melatonin via s.c. injection (1 mg x kg(- 1) body weight x day(- 1)). At the end of experiment, all animals were sacrificied by decapitation, serum and tissue samples were removed for determination of malondialdehyde (MDA), a product of lipid peroxidation, conjugated dienes levels and glutathione peroxidase (GSH-Px) activity levels. It was found that lipid peroxidation was increased in the rats which were exposed to constant light. Melatonin injection caused a decrease in lipid peroxidation, especially in the brain. In addition, melatonin application resulted in increased GSH-Px activity, which has an antioxidant effect. Thus, melatonin is not only a direct scavenger of toxic radicals, but also stimulates the antioxidative enzyme GSH-Px activity to detoxify hydroxyl radical produced by constant light exposure.</p