Phycobiliproteins extract from Spirulina protects against single-dose cadmium-induced reproductive toxicity in male mice

Environmental Science and Pollution Research - Cadmium (Cd) is known for its many toxic effects on male population such as hypogonadism and fertility difficulties, which are oftenly associated with...     

Does static electric field from ultra-high voltage direct-current transmission lines affect male reproductive capacity? Evidence from a laboratory study on male mice

With the development of ultra-high-voltage direct-current (UHVDC) transmission technology and increase in transmission voltage, the issue of environmental static electric field (SEF) pollution is standing out and its possible health effects have caused much public attention. In this study, the effects of chronic exposure to SEF on reproductive capacity of male mice were investigated. Twenty Institute of Cancer Research (ICR) mice were exposed to SEF (56.3 ± 1.4 kV/m, 49 days) generated by a high-voltage device. Several biological end points related to spermatogenesis and testicular function were evaluated, including reproductive organ coefficients, sperm motility and morphology, serum testosterone level, and testicular histology. No significant differences were found between the SEF-exposed and sham-exposed groups at the end of the exposure period. However, further observation through transmission electron microscopy revealed cristae losses in mitochondria of spermatogenic cells after SEF exposure. Nevertheless, the mitochondria injury did not affect sperm motility, which might be explained from the perspective of energy supply. That is, most of the energy required for sperm movement is generated by glycolysis which occurs in the cytoplasm rather than oxidative phosphorylation which occurs in mitochondria. In conclusion, this study indicates that exposure to SEF (56.3 ± 1.4 kV/m, 49 days) has limited effects on male reproductive capacity.     

Constant light exposure and/or pinealectomy increases susceptibility to trichloroethylene-induced hepatotoxicity and liver cancer in male mice

Environmental Science and Pollution Research - Exposure to light at night, pineal gland impairment, and the environmental pollutant trichloroethylene (TCE) have serious implications for health and...     

Effects of perinatal exposure to bisphenol A and di(2-ethylhexyl)-phthalate on gonadal development of male mice

Purpose

In this study, we investigated the effects of maternal transfer of bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) during gestational and weaning periods on gonadal development of male offspring.

Methods

Pregnant CD-1 mice were administered by gavages in corn oil with 0.1, 1, or 10 mg/kg/day of BPA and DEHP from gestational days (GD1?C21) to the weaning period (postnatal days (PND) 1?C21).

Results

Our data indicated that the exposure significantly reduced the male-to-female sex ratio and the sizes of the gonads of male pups as recorded at PND15. The testes of the perinatally exposed male pups were developed less and the expression levels of testicular anti-mullerian hormone, androgen receptor, cyclin A, and StAR were significantly lesser than the control male pups. The less developed testes were accompanied with significant reductions in the expression levels of Gnrh and Fsh at the hypothalamic?Cpituitary levels. The negative effects were found to be persistent in the sexually mature pups at PND42.

Conclusion

Our data reveal that the maternal transfer of BPA and DEHP may impose negative influence on the development and functions of the reproductive system of male pups.     

Chronic depression-like phenotype in male offspring mice following perinatal exposure to naturally contaminated eels with a mixture of organic and inorganic pollutants

Previously, we demonstrated that maternal exposure to high, intermediate, or lowly contaminated European eels with a mixture of chemicals, during pregnancy and lactation, resulted in adult despair-like behavior, selectively in male offspring mice. Here, we investigate if depression-like behavior in offspring males was transient or permanent by monitoring immobility behavior, a measure of behavioral despair, at three distinct stages of life, including young adult (post-natal day (PND) 55), mature adult (PND 200) and middle (PNDs 335–336) age, in the forced swimming (FST) and the tail suspension (TST) tests. Oxidative stress markers including malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities were evaluated in the hippocampus, prefrontal cortex, and cerebellum of middle-aged animals. Findings showed a significant enhancement of immobility behavior in the TST performed at young adult age (all p < 0.05) in the FST carried out at mature adult age (all p < 0.001) and in both behavioral tests realized at middle age (all p < 0.05, except one p = 0.06) in mice perinatally exposed to eels compared with non-exposed controls. Antioxidant-related enzyme activities, including SOD and CAT, were only elevated in the hippocampus of middle-aged males perinatally exposed to the two more polluted eels (all p < 0.05). Further, lipid peroxidation, assessed by MDA levels, was not found to be differentially regulated in the selected areas of middle-aged brains of exposed mice (all p > 0.05). Collectively, this suggested limited oxidative metabolism disturbances in middle-aged brains exposed to eels. In summary, our results highlighted that offspring males perinatally exposed to naturally contaminated reared and river eels with persistent organic pollutants (POPs) and heavy metals displayed chronic depression-like phenotype. As extrapolation of data to humans should be done with precaution, retrospective and prospective epidemiological studies are needed to clarify this potential relationship, stressed in our animal model, between maternal polluted fish consumption and chronically low mood in offspring.

     

In vivo studies on the effect of some insecticides on the hepatic activities of L-tryptophan 2,3-dioxygenase and pyridoxal phosphokinase of male mice

The effect of Dimethoate, Carbaryl and Permethrin on the activities of liver L-tryptophan 2,3-dioxygenase (total-, holo-, and apo-forms) and pyridoxal phosphokinase of male mice was investigated. Dimethoate inhibited both enzyme systems after single and repeated dose treatment; except the dioxygenase holo-enzyme after repeated doses. Single dose of Carbaryl treatment inhibited the pyridoxal phosphokinase, total and holo-enzyme of L-tryptophan dioxygenase. However, the repeated dose treatment do not affect both enzyme systems. Permethrin inhibited only total-, holo- and apo-enzymes of L-tryptophan dioxygenase whereas repeated administration has no significant effect on both enzymes. The data indicate that these insecticides may induce abnormal tryptophan metabolism through which some endogenous bladder carcinogens are formed.     

Thiram-induced toxic liver injury in male Sprague-Dawley rats

A single i.p. dose (120 mg/kg) of thiram given to male Sprague-Dawley rats caused a significant increase in the activity of SGOT and SGPT 24 hr post-treatment indicating liver damage. A considerable diminution in the serum cholinesterase activity was also noted in the treated rats as against the control animals. Additional evidence for thiram-induced liver toxicity is provided by the observation that there was approximately 50% inhibition of the activity of hepatic microsomal benzphetamine N-demethylase with a concomitant decrease in the concentration of cytochrome P-450, an important component of the mixed-function oxidase system. Although not significant, hepatic glutathione levels were also depleted by thiram, probably making the liver susceptible to toxic injury.     

The mutagenic effect of tobacco smoke on male fertility

Despite the association between tobacco use and the harmful effects on general health as well as male fertility parameters, smoking remains globally prevalent. The main content of tobacco smoke is nicotine and its metabolite cotinine. These compounds can pass the blood-testis barrier, which subsequently causes harm of diverse degree to the germ cells. Although controversial, smoking has been shown to cause not only a decrease in sperm motility, sperm concentration, and an increase in abnormal sperm morphology, but also genetic and epigenetic aberrations in spermatozoa. Both animal and human studies have highlighted the occurrence of sperm DNA-strand breaks (fragmentation), genome instability, genetic mutations, and the presence of aneuploids in the germline of animals and men exposed to tobacco smoke. The question to be asked at this point is, if smoking has the potential to cause all these genetic aberrations, what is the extent of damage? Hence, this review aimed to provide evidence that smoking has a mutagenic effect on sperm and how this subsequently affects male fertility. Additionally, the role of tobacco smoke as an aneugen will be explored. We furthermore aim to incorporate the epidemiological aspects of the aforementioned and provide a holistic approach to the topic.

     

Juvenile hormone agonists affect the occurrence of male Daphnia

The water flea Daphnia magna reproduces primarily by cyclic parthenogenesis. Environmental stimuli that signal a change to adverse conditions induce the organisms to switch from parthenogenesis to gamogenetic reproduction. During the gamogenetic period, they produce male daphnids and dormant resting eggs, which can survive prolonged periods of environmental adversity. However, little is known about the mechanisms associated with the switch from parthenogenesis to gamogenetic reproduction. We investigated the effects of several juvenoids on sex determination in Daphnia. Females less than 24 h old were exposed to various concentrations of the test substance and were observed for 21 days. It was found that they can trigger the appearance of male daphnids: the percentage of males in the population increases to a level greater than what occurs under ordinary environmental conditions. We found that methylfarnesoate, juvenile hormone III, methoprene, and the phenoxyphenoxy derivatives pyriproxyfen and fenoxycarb (both insecticides) reduced the production of offspring and produced sex ratios dominated by male daphnids. Pyriproxyfen and fenoxycarb showed striking effects at low concentrations. Exposure to either of these chemicals at a concentration of 330 ngl(-1) caused adult females to produce almost all male neonates. Methylfarnesoate, juvenile hormone III, and methoprene showed an effect in inducing male production at higher concentrations (3.7 x 10(3), 3.3 x 10(5), and 1.3 x 10(5) ngl(-1), respectively). Our findings suggest that juvenile hormone agonists, including some insecticides, affect the chemical signaling responsible for inducing the production of male offspring.     

Effects of phosphorothionate on the reproductive system of male rats

Acute and Sub-acute toxic effects of a new pesticide phosphorothionate coded as RPR-V on testis of albino rat were studied. For the acute study, rats received a single dose of 30 mg/kg of RPR-V and sacrificed after 24 hours. For the Subacute study, 1.42 mg/kg/day was administered orally to rats for 10 days and 21 days. Acute exposure of rats to RPR-V brought no change either in the Gonadosomatic Index (GSI) or in the structure of testis or in the serum levels of Testosterone. Similarly, no significant change was observed in the Glutathione S-transferase (GST) activity. But, in testis there was significant increased in the reduced Glutathione (GSH) and Acid Phosphatase (AcP), whereas Alkaline Phosphatase (AkP) levels decreased significantly at 24hr post treatment. On 7th day (withdrawal period) after the cessation of the treatment the GSH, AcP, and AkP levels reached to near control. The sub-acute study revealed a significant post treatment. Due to RPR-V treatment the testis AcP levels increased significantly at 21st day of medication but AkP levels decreased both at 10th and 21st day of post treatment. Histopathological studies showed that after 10th day testis showed considerable loss of spermatozoids and at 21st day complete derangement of cellular organization was observed. Testosterone levels decreased significantly after 10th day and remained significantly low at 21st day. However, withdrawal studies showed a recovery in testis of rat treated with RPR-V. GST, GSH, GSI, AcP and AkP values were recovered, testosterone levels were also recovered but recovery in testis structure remained at a low profile.     

Developmental exposure to diuron causes splenotoxicity in male Sprague-Dawley rat pups

This study investigated whether perinatal exposure to diuron [3-(3,4-dichlorophenyl)-1-1-dimethylurea] might exert adverse effects on rat lymphoid organs. Pregnant Sprague-Dawley (SD) rats were exposed to diuron at 500, 750 or 1250 ppm in the diet from gestational days (GD) 12-21 and during lactation. At postnatal day (PND) 42, male pups were euthanized and thymus, spleen, mesenteric lymph node and femur were collected for histopathological analysis. Food consumption and body weight gain were significantly reduced in dams exposed to 1250 ppm during gestation period. Also, Diuron at 750 and 1250 ppm produced: (1) increased relative spleen weight associated histologically with severe congestion in red pulp, (2) enhanced extramedullary hematopoiesis and hemosiderosis as well as (3) depletion of lymphoid follicles in white pulp. Flow cytometric analysis revealed a significant reduction in B lymphocytes (CD45RA+) in male pups but T lymphocytes (CD4+, CD8+ and CD4+/CD8+) were not markedly affected. Thus, data suggest that Diuron-induced maternal toxicity in dams exposed to high dose and perinatal exposure to this herbicide produced spleen toxicity as evidenced by a reduction in B lymphocyte number in male SD pups.     

Developmental exposure to diuron causes splenotoxicity in male Sprague-Dawley rat pups

This study investigated whether perinatal exposure to diuron [3-(3,4-dichlorophenyl)-1-1-dimethylurea] might exert adverse effects on rat lymphoid organs. Pregnant Sprague-Dawley (SD) rats were exposed to diuron at 500, 750 or 1250 ppm in the diet from gestational days (GD) 12–21 and during lactation. At postnatal day (PND) 42, male pups were euthanized and thymus, spleen, mesenteric lymph node and femur were collected for histopathological analysis. Food consumption and body weight gain were significantly reduced in dams exposed to 1250 ppm during gestation period. Also, Diuron at 750 and 1250 ppm produced: (1) increased relative spleen weight associated histologically with severe congestion in red pulp, (2) enhanced extramedullary hematopoiesis and hemosiderosis as well as (3) depletion of lymphoid follicles in white pulp. Flow cytometric analysis revealed a significant reduction in B lymphocytes (CD45RA+) in male pups but T lymphocytes (CD4+, CD8+ and CD4+/CD8+) were not markedly affected. Thus, data suggest that Diuron-induced maternal toxicity in dams exposed to high dose and perinatal exposure to this herbicide produced spleen toxicity as evidenced by a reduction in B lymphocyte number in male SD pups.     

Subacute oral toxicity of BDE-15, CDE-15, and HODE-15 in ICR male mice: assessing effects on hepatic oxidative stress and metals status and ascertaining the protective role of vitamin E

The present study examined the effects of oral exposure of 4,4′-dibromodiphenyl ether (BDE-15), 4,4′-dichlorodiphenyl ether (CDE-15), and 4,4′-dihydroxydiphenyl ether (HODE-15) on hepatic oxidative stress (OS) and metal status in Institute of Cancer Research (ICR) male mice. Furthermore, the role of vitamin E in ameliorating potential OS caused by BDE-15, CDE-15, and HODE-15 was investigated. Three groups of mice were exposed to 1.20 mg/kg(body weight)/day of each of the three toxicants for 28 days. Results showed that none of the three toxicants altered growth rates of mice, but significantly increased (P?<?0.05) relative liver weights and decreased relative kidney weights. Pathological changes including cell swelling, inflammation and vacuolization, and hepatocellular hypertrophy in livers were observed. Significant decreases (P?<?0.05 and P?<?0.01) in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and glutathione (GSH) levels, together with increases in malondialdehyde (MDA) content were recorded in all toxicant-treated groups. Hepatic copper levels increased in all toxicant-treated groups. Hepatic zinc levels decreased in the liver of BDE-15-treated mice, whereas they increased in the livers of CDE-15-treated and HODE-15-treated mice. In conclusion, daily exposure to the three toxicants perturbed metal homeostasis and increased OS in mouse liver. Experimental data indicated the hepatic oxidative toxicity of the three toxicants followed the order BDE-15?<?HODE-15?<?CDE-15. Moreover, the study proved that daily supplementation of 50 mg/kg vitamin E is effective to ameliorate the hepatic OS status and metal disturbance in mice.     

Pharmacokinetic profile and anticholinesterase properties of phenamiphos in male rats.

The pharmacokinetics and anticholinesterase properties of a single oral dose 6 mg/Kg of technical phenamiphos [ethyl 4-(methylthio)-m-tolyl isopropylphosphoramidate] were investigated in male rats. Animals were killed at each time intervals of 0.5, 1.0, 1.5, 3, 6, 12, 24, 48, and 72 hrs after dosing. The total recovered amount of phenamiphos from brain and plasma tissues reached high level at the first time interval and disappeared biexponentially from both tissues to low level at the end of the experiment. Brain tissue has a greater affinity to phenamiphos than plasma tissue. The half-life of the elimination of phenamiphos from brain and plasma were 100 and 212 hr corresponding to the rate constant values of 0.01 and 0.003 hr-1, respectively. Plasma AUC (area under the curve) value was 1239.81 micrograms hr/L, explaining there was no tendency for the compound to accumulate in the brain tissue (AUC = 774.38 micrograms hr/Kg) compared to the plasma. On the other hand, determination of cholinesterase activity showed that, phenamiphos inhibited the enzymes in both brain and plasma, where the depression of ChE activity was usually more marked in plasma than in brain.     

Assessment of imidacloprid toxicity on reproductive organ system of adult male rats

In the current study it was aimed to investigate the toxicity of low doses of imidacloprid (IMI) on the reproductive organ systems of adult male rats. The treatment groups received 0.5 (IMI-0.5), 2 (IMI-2) or 8 mg IMI/kg body weight by oral gavage (IMI-8) for three months. The deterioration in sperm motility in IMI-8 group and epidydimal sperm concentration in IMI-2 and IMI-8 groups and abnormality in sperm morphology in IMI-8 were significant. The levels of testosterone (T) and GSH decreased significantly in group IMI-8 compared to the control group. Upon treatment with IMI, apoptotic index increased significantly only in germ cells of the seminiferous tubules of IMI-8 group when compared to control. Fragmentation was striking in the seminal DNA from the IMI-8 group, but it was much less obvious in the IMI-2 one. IMI exposure resulted in elevation of all fatty acids analyzed, but the increases were significant only in stearic, oleic, linoleic and arachidonic acids. The ratios of 20:4/20:3 and 20:4/18:2 were decreased and 16:1n-9/16:0 ratio was increased. In conclusion, the present animal experiments revealed that the treatment with IMI at NOAEL dose-levels caused deterioration in sperm parameters, decreased T level, increased apoptosis of germ cells, seminal DNA fragmentation, the depletion of antioxidants and change in disturbance of fatty acid composition. All these changes indicate the suppression of testicular function.     

Bone mineral density in male Baltic grey seal (Halichoerus grypus)

Bone mineral density (mg cm(-3)) was studied in male Baltic grey seals (4-23 years of age) by noninvasive computed tomography (pQCT). The material was grouped according to year of collection. Group A: 1850-1955, a period before the main introduction of organochlorines (OCs); Group B: 1965-1985, a period with very high OC contamination; and Group C: 1986-1997, a period with decreasing concentrations of OCs. The reproducibility of the measurements was good with a Coefficient of Variation (CV) ranging from 0.1% to 2.1%. Trabecular bone mineral density of the radius was significantly higher in specimens collected 1986-1997 than in those collected 1965-1985 (p < 0.05). Cortical bone mineral density of the mandible was significantly lower in specimens collected 1986-1997 compared with those collected 1850-1955 (p < 0.05). These results indicate different responses over time in trabecular and cortical bone. During the period of very high OC contamination (1965-1985), trabecular bone density was lowest, whereas cortical bone density was lowest in specimens collected 1985-1997, representing a period of fairly low OC contamination. The mechanisms behind these effects are not known. However, it can be assumed that OCs are involved. Information about residue levels of OCs in the studied individuals is lacking and, therefore, it was not possible to evaluate the impact of OCs in this respect.     

Thiram‐induced toxic liver injury in male sprague‐dawley rats

Abstract

A single i.p. dose (120 mg/kg) of thiram given to male Sprague‐Dawley rats caused a significant increase in the activity of SGOT and SGPT 24 hr post‐treatment indicating liver damage. A considerable diminution in the serum cholinesterase activity was also noted in the treated rats as against the control animals. Additional evidence for thiram‐induced liver toxicity is provided by the observation that there was approximately 50% inhibition of the activity of hepatic microsomal benzphetamine N‐demethylase with a concomitant decrease in the concentration of cytochrome P‐450, an important component of the mixed‐function oxidase system. Although not significant, hepatic glutathione levels were also depleted by thiram, probably making the liver susceptible to toxic injury.     

Environmental pollutants: genetic damage and epigenetic changes in male germ cells

About a quarter of the human diseases occurs for exposure to air pollution. The male reproductive system, and especially spermatogenesis, seems to be particularly sensitive. As result, male infertility is increasing in industrial countries becoming a top priority for public health. In addition to psychological distress and economic constraints, poorer semen quality may have trans-generational effects including congenital malformations in the offspring and predispose to later onset adult diseases. Genetic and epigenetic alterations are involved in the failure of spermatogenesis. In this paper, we reviewed the major evidences of the effects of air pollutants on male infertility as well as the role of sperm DNA damage and epigenetic changes in affecting spermatogenesis. A better knowledge on the effects of air contaminants on the molecular mechanisms leading to infertility is of huge importance to help clinicians in identifying the cause of infertility but above all, in defining preventive and therapeutic protocols.