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Twenty-four hour changes of serotonin content in the median eminence (a), anterior pituitary (b), and posterior pituitary (c), in control and cadmium-treated animals. Groups of 10 rats were killed by decapitation at six different time intervals throughout a 24 h cycle. Shown as the means ± S.E.M. Letters indicated the existence of significant differences between time points within each experimental group after a Tukey-Kramer's multiple comparisons tests, as follows-(a): a p < 0.001 vs. 08:00, 12:00, 20:00, and 00:00 h; b p < 0.001 vs. 08:00, 12:00, 20:00, and 00:00 h; c p < 0.01 vs. 08:00 h; (b): a p < 0.001 vs. all time points; b p < 0.05 vs. 12:00 and 00:00 h; (c): a p < 0.001 vs. all time points. For further statistical analysis, see text.
Source publication
This work was designed to analyze the effects of cadmium on the regulatory mechanism of prolactin in cadmium-exposed rats. Adult male rats were given cadmium at a dose of 25 ppm of cadmium chloride (CdCl2) in the drinking water for 1 month. At the end of the treatment, the rats were killed at six different time intervals throughout a 24 h cycle to...
Contexts in source publication
Context 1
... effects of oral cadmium exposure on the 24 h serotonin content in the median eminence are shown in Fig. 3a. There were specific 24 h variations in sero- tonin content in both control (F = 20.41, p < 0.001) and metal-exposed rats (F = 3.58, p < 0.01) in the me- Table 1 Correlation between dopamine content in the median eminence and anterior pituitary, and between serotonin content in the median eminence and anterior pituitary, in adult male ...
Context 2
... 12:00 h. Although mean concentration of serotonin did not change in cadmium-exposed animals, serotonin content in this region diminished at 16:00 and 04:00 h (p < 0.001), and increased at 00:00 h (p < 0.05). There was an interaction between cadmium treatment and time of the day as far as serotonin in the median emi- nence (F = 10.37, p < 0.001) (Fig. 3a). The effects of oral cadmium administration on the 24 h serotonin content in the anterior pituitary are shown in Fig. 3b. Serotonin content in the anterior pi- tuitary changed as a time of the day in both control (F = 17.34, p < 0.001) and cadmium-exposed animals (F = 34.49, p < 0.001). The pattern of serotonin content in the control ...
Context 3
... diminished at 16:00 and 04:00 h (p < 0.001), and increased at 00:00 h (p < 0.05). There was an interaction between cadmium treatment and time of the day as far as serotonin in the median emi- nence (F = 10.37, p < 0.001) (Fig. 3a). The effects of oral cadmium administration on the 24 h serotonin content in the anterior pituitary are shown in Fig. 3b. Serotonin content in the anterior pi- tuitary changed as a time of the day in both control (F = 17.34, p < 0.001) and cadmium-exposed animals (F = 34.49, p < 0.001). The pattern of serotonin content in the control group was characterized by the existence of a two peaks (20:00 and 04:00 h) during the light and the dark phase of the ...
Context 4
... in 24 h serotonin content in the posterior pituitary induced by oral cadmium administration is shown in Fig. 3c. Serotonin content in the posterior pituitary changed as a time of the day in both control (F = 15.78, p < 0.001) and cadmium-exposed animals (F = 7.77, p < 0.001). The pattern of serotonin con- tent in the control group was characterized by the exis- tence of a single peak (00:00 h) during the dark phase of the photoperiod. In ...
Citations
... More specifically, taurine depletion can occur during arsenic-induced cardiomyocyte viability, reactive oxygen species products, intracellular calcium, and apoptotic cell death (Flora et al., 2014). Taurine has also been observed to reduce cadmium-indices damages in murine hearts (Manna et al., 2008) and hypothalamus (Lafuente et al., 2005). A similar effect is exhibited in rats with taurine and its hepatoprotective effects against mercury toxicosis (Samipillai et al., 2010). ...
Dilated cardiomyopathy (DCM) has been in the literature and news because of the recent opinion-based journal articles and public releases by regulatory agencies. DCM is commonly associated with a genetic predisposition in certain dog breeds and can also occur secondary to other diseases and nutritional deficiencies. Recent communications in veterinary journals have discussed a potential relationship between grain-free and/or novel protein diets to DCM, citing a subjective increase in DCM in dog breeds that are not known to have a genetic predisposition for the disease. This literature review describes clinical presentations of DCM, common sequelae, treatment and preventative measures, histopathologic features, and a discussion of the varied etiological origins of the disease. In addition, current literature limitations are addressed, in order to ascertain multiple variables leading to the development of DCM. Future studies are needed to evaluate one variable at a time and to minimize confounding variables and speculation. Furthermore, to prevent sampling bias with the current FDA reports, the veterinary community should be asked to provide information for all cases of DCM in dogs. This should include cases during the same time period, regardless of the practitioner’s proposed etiology, due to no definitive association between diets with specific characteristics, such as, but not limited to, grain-free diets and those containing legumes, novel protein diets, and those produced by small manufacturers to DCM in dogs. In summary, in order to determine if certain ingredients, categories of diets, or manufacturing processes are related to an increased risk of DCM, further studies investigating these variables are necessary.
... The role of Hg is only one of the hypothetic causative agents in the dopamine-related dysfunctions leading to PD [56,57]. And the activity of mixed exposures to toxic metals is particularly complex, as it may not be described merely by a classical dose-response mechanism [58]. Therefore, further research is requested to elucidate the etiopathogenetic role of metal pollutants in PD. ...
... Particularly, nigral dopaminergic neurons are very sensitive to Hg because of elevated glutamate toxicity and their high content of tubulin [56]. PD onset has been associated with exposure to elevated levels of Hg [58]. Numerous similarities between the effects of Hg ingestion/ exposure and the consequences/symptoms of patients with PD have been reported, although Hg has not only been related to the PD incidence [56]. ...
Research on the etiopathogenesis of Parkinson’s disease (PD) has in the very recent years earned many insightful cues about the involvement of xenobiotics and metal pollutants in the onset and exacerbation of this neurodegenerative disorder. Furthermore, particularly for metal pollutants, the hypothesis about the role exerted by impaired mitochondrial function is gaining a leading causative role. In this review, we outline the role of environmental pollution in the pathogenesis of PD, as the prolonged exposure to xenobiotics may account for the majority of PD reported cases, expanding the debate also about some suggested therapeutic approaches.
... 3×1 0 −9 M Nucleus Accumbens Rat Microdialysis (Hernandez and Hoebel 1988) 9.75 nM 9.8 × 10 −9 M Nucleus Accumbens Rat Microdialysis (Pettit et al. 1990) 58.7 fmol/40 μl 1.5×10 −9 M Nucleus Accumbens Rat Microdialysis (Fadda et al. 2003) 0.59 pg/μl c 3.9 × 10 −9 M a Nucleus Accumbens (Shell) Rat Microdialysis (Adachi et al. 2013) 0.884 nmol/g 8.8 × 10 −7 M a Occipital Cortex Primate HPLC (Elchisak et al. 1983) 40.6 ng/g 2.7 × 10 −7 M a Olfactory Bulb Mouse LC-MS 0.192 μg/g 1.3 × 10 −6 M a Olfactory Bulb Primate HPLC (Pifl et al. 2017) 75 pg/mg b 4.9 × 10 −7 M a Olfactory Bulb Rat HPLC (Bromek et al. 2011) 6.87 nmol/g 6.9 × 10 −6 M a Olfactory Cortex Primate HPLC (Elchisak et al. 1983) 11 ng/g 7.1 × 10 −8 M a Olfactory Tubercle Human HPLC (Musshoff et al. 2000) 0.34 μM 3 . 4×1 0 −7 M Olfactory Tubercle Rat FSCV (Wakabayashi et al. 2016) 4.1 ng/mg c 2.7 × 10 −5 M a Olfactory Tubercle Rat HPLC (Bradbury et al. 1985) 39.7 ng/mg c 2.6 × 10 −4 M a Olfactory Tubercle Rat Radioenzymatic Assay (Demarest et al. 1982) 6 ng/mg b 3.9 × 10 −5 M a Paraventricular Nucleus Mouse HPLC (Sakic et al. 2002) 14 (Nagy et al. 1998) 6 pg/μg b 3.9 × 10 −5 M a Pituitary Gland (Posterior) Rat HPLC (Lafuente et al. 2005) 7.8 ng/mg c 5.1 × 10 −5 M a Pituitary Gland (Posterior) Rat Radioenzymatic Assay (Demarest et al. 1982) 0.176 nmol/g 1.8 × 10 −7 M a Pons Primate HPLC (Elchisak et al. 1983) 0.1 pmol/mg 1 × 10 −7 M a Postcentral Gyrus Human HPLC (Ebinger et al. 1987) 15 ng/g 9.8 × 10 −8 M a Precentral Gyrus Human HPLC (Musshoff et al. 2000) 0.08 pmol/mg 8 × 10 −8 M a Precentral Gyrus Human HPLC (Ebinger et al. 1987) 113 (SbN), where dopaminergic neurons give rise to ascending fibers densely innervating the caudate and putamen (dorsal striatum). Both the mesolimbic pathway and mesocortical pathways are associated with the reward system (Wise 2004). ...
Dopamine is well recognized as a neurotransmitter in the brain, and regulates critical functions in a variety of peripheral systems. Growing research has also shown that dopamine acts as an important regulator of immune function. Many immune cells express dopamine receptors and other dopamine related proteins, enabling them to actively respond to dopamine and suggesting that dopaminergic immunoregulation is an important part of proper immune function. A detailed understanding of the physiological concentrations of dopamine in specific regions of the human body, particularly in peripheral systems, is critical to the development of hypotheses and experiments examining the effects of physiologically relevant dopamine concentrations on immune cells. Unfortunately, the dopamine concentrations to which these immune cells would be exposed in different anatomical regions are not clear. To address this issue, this comprehensive review details the current information regarding concentrations of dopamine found in both the central nervous system and in many regions of the periphery. In addition, we discuss the immune cells present in each region, and how these could interact with dopamine in each compartment described. Finally, the review briefly addresses how changes in these dopamine concentrations could influence immune cell dysfunction in several disease states including Parkinson’s disease, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, as well as the collection of pathologies, cognitive and motor symptoms associated with HIV infection in the central nervous system, known as NeuroHIV. These data will improve our understanding of the interactions between the dopaminergic and immune systems during both homeostatic function and in disease, clarify the effects of existing dopaminergic drugs and promote the creation of new therapeutic strategies based on manipulating immune function through dopaminergic signaling.
Graphical Abstract
... 21 Caride et al. 22 showed that the alteration of BBB integrity by Cd increases dopamine levels and decreases gamma-aminobutyric acid (GABA) levels in different brain regions. Serotonin levels increased in adenohypophysis and neurohypophysis in rats treated with Cd. 23 The high concentration of glutamate neurotransmitters becomes neurotoxic and is involved in neurodegenerative diseases, including AD. 24 The increase in glutamate levels causes enlightened depletion, reduced GSH and subsequent oxidative stress. 25 Amyloid beta protein (Ab) is found in the brain and cerebrospinal fluid of humans with good cognitive function and memory throughout their life. ...
... 70,71 Moreover, Cd alters gamma-Aminobutyric acid (GABAergic) and glutamatergic pathways, dopamine 45 and serotonin concentration in rats administered with Cd as in Figure 6. 23 The neurotoxic effect of Cd in experimental animals is due to its impairment of catecholaminergic and serotoninergic transmission. 5 Therefore, it has been postulated that Cd-induced blockage of cholinergic transmission in the brain is mediated by high AChE activity. ...
Because cadmium (Cd) is not naturally degradable by ecosystems, it interferes with many types of food chains. Cd accumulates in the kidney, liver and in the nervous tissues, especially the brain. The neurotoxicity of Cd is very high, as it alters the integrity, and increases the permeability, of the blood–brain barrier. Cd penetrates and accumulates in neurons in the brains of rats. This study reveals that Cd decreases antioxidant enzymes and increases oxidative stress in the brain. In addition, Cd increases lipid peroxidation of brain tissues. Cd increases the expression of the Cu/Zn superoxide dismutase gene. It also affects cholinergic, glutamatergic, gamma-Aminobutyric acid (GABAergic), dopamine, serotonin and acetylcholine neurotransmitters in brain tissue. Consequently, Cd increases the formation of amyloid β, a neurotoxic index, and induces apoptosis by changing the quality and the quantity of Bcl-2, Bax and p53 proteins. In conclusion, both selenium and nanoselenium show potential antioxidant activity and promote recovery from the neurotoxic action of Cd.
... E xposur e t o lea d ca n cause en docri n e disturbances and affect hormone systems by interfering mainly with steroid hormones (Lafuente et al., 2005) as the gonads are affected by lead exposure (Rana, 2014). Lead was observed to reduce adrenocorticotrophic hormone (ACTH)-induced steroid production in cultured cells (Nishiyama et al., 1985). ...
... These results clearly showed that lead has adverse effect on hepatic, renal and muscle tissue which is in accordance with the previous reports (El-Nekeety et al., 2009 andMohajeri et al., 2014). Lead is known to interfere with steroid and thyroid hormone systems (Lafuente et al., 2005). Exposure to low level of heavy metals impairs the glucocorticoid system (Kaltreider et al., 2001). ...
Lead emitting industries pose a risk of contamination of surface and ground water, soil and fodder by dissemination of the particles carrying lead by wind action and by runoff from the tailings which cause numerous biochemical, immunological and reproductive disturbances in animals. Samples (n-20) of tube-well water, surface soil and fodder were collected from an uncontaminated area with water lead level within the permissible limit (0.05µg/ml) which served as control, and from the lead contaminated area (n=25) of Ludhiana (Punjab) with water lead level above the permissible limit. Blood level of lead (>0.24µg/ml) was used to decide the exposure group. The biochemical profile of the buffaloes exposed to lead showed hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypertriglyridemia and hyperglycemia as compared to control group. The activity of serum enzymes viz alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase, alkaline phosphatase, lactate dehydrogenase and creatine kinase showed significant (p less than 0.05) elevation in lead exposed buffaloes. There was significant (p less than 0.05) increase in levels of plasma urea and creatinine, however, tri-iodothyrinine and thyroxine concentrations were significantly (p less than 0.05) declined in lead exposed buffaloes as compared to control animals. Blood lead levels were significantly correlated with alterations in different biochemical indices in lead exposed buffaloes indicating the adverse effect on hepatic, renal and thyroid function.
... [4] Lungs disorders are dominant in workers who are exposed to cadmium. [4,[13][14][15][16][17][18] Though cadmium is considered a potent occupational risk factor, less attention has been paid to its neurotoxic effects. Different types of cells respond to the same toxic material differently. ...
Background
Cadmium is a nonessential toxic heavy metal, which enters the body easily and damages the cellular system. The sonic hedgehog (Shh) signaling pathway is one of the key regulatory pathways, which define neural growth and development.
Objectives
This study aimed to explore how cadmium exposure affects neural activities, Shh signaling cascade, and its downstream target genes.
Methods
Total 18 male Wistar rats were randomly divided into two groups, control and test groups. Test rats were administered with 3 mg cadmium/kg body weight, while the control rats were treated with vehicle continuously for 28 days. Thereafter, rats were killed and the isolated brain samples were examined using oxidative stress assessment, histological and immunohistological behavioral assessment, polymerase chain reaction (PCR), and the comet assay.
Results
A disturbed oxidative balance, DNA damage, and an upregulated Shh signaling pathway were observed in cadmium‐treated samples. Loss of structural integrity in cerebellum and loss of motor activity were observed in cadmium‐treated rats.
... The presence of cadmium in the brain and its neurotoxic properties disrupt the synthesis and secretion of neurotransmitters in the hypothalamus and pituitary gland of the rat (Pillai et al. 2003;Lafuente et al. 2005). Changes in the release of LH gonadotropin from the pituitary gland under the influence of cadmium were also observed in our study. ...
... Numerous studies conducted on mammals confirm that cadmium affects the activity of the hypothalamus and the pituitary gland. The inhibiting effect of cadmium on releasing biogenic amines from the hypothalamus of the rat has been demonstrated by many authors (Pillai et al. 2003;Lafuente et al. 2005;Romero et al. 2011). Cadmium indirectly stimulates the release of LH from the pituitary gland by inhibiting the release of dopamine, functioning as a gonadotropin release-inhibiting factor in fish. ...
The aim of this study was to determine whether melatonin (Mel), which is a known antioxidant and free radical scavenger, could perform the role of a preventive agent against the toxic effects of cadmium (Cd²⁺) on mortality, fish growth, gonadosomatic index (GSI), luteinizing hormone (LH) secretion, the response to hormonal stimulation of spawning, and also tissue accumulation of Cd in Prussian carp females. These females received melatonin implants and were exposed to 0.4 or 4.0 mg/L of Cd (as CdCl2·2.5H2O) over either a 5- or 3-month period, followed by further 2 months of purification in clear water. Negative changes caused by exposure to cadmium in the water were as follows: higher fish mortality, lower body weight, increased accumulation of cadmium in the brain and ovary, lowered GSI, impaired spontaneous LH secretion during exposure, and impaired LH secretion during stimulation of spawning. All of these effects were observed in the group of fish exposed to 0.4 and/or 4.0 mg Cd/L but did not occur or were less pronounced in the groups exposed to cadmium in the presence of melatonin released from the implants. During depuration, in the group of fish which had been exposed to the highest Cd concentration, we observed a significant improvement in fish survival rate, body growth, inhibition of further cadmium accumulation in tissues, and gradual return of spontaneous LH secretion as well as normalization of the GSI value to the control group levels. In conclusion, these findings indicate that melatonin can be a preventive agent for some toxic effects on fish reproduction induced by environmental cadmium contamination.
Electronic supplementary material
The online version of this article (10.1007/s11356-018-1308-8) contains supplementary material, which is available to authorized users.
... Bhalla et al. (2007) reported that orally administered Zn did not cause a significant alteration in serotonin concentration. Lafuente et al. (2005) reported that rats exposed to Cd had no change in 5-HT concentration in the median eminence, although it increased in both the anterior and posterior pituitary. ...
... These results support the theory that Zn supplementation can reduce the suppressive effect exerted by heavy metals on dopamine synthesis. Cd and Pb can cross the blood-brain barrier and reduce the concentrations of this amine (Lafuente et al., 2005;Romero et al., 2011). In rats exposed to Cd, dopamine levels increased in the posterior pituitary but decreased in the median eminence (Lafuente et al., 2003). ...
... The reduction in weight gain could have been due to the decrease in food intake, or due to the overall increased degeneration of lipids and proteins as a result of cadmium toxicity (Erdogan et al. 2005). Also, Lafuente et al. (2005) reported that cadmium inhibits the activity of glutathione peroxidase and glutathione reductase, which indicates that cadmium can promote depletion of glutathione and inhibit production of it, and this is associated with the reduce in growth rate. Antioxidants mitigate the free radical-induced cellular damage through various modes which include, suppression of hydroperoxides and hydrogen peroxides, averting the propagation of peroxidative chain reaction, or by clearing away the active free radicals (Sen et al. 2010). ...
Toxic and apoptotic impacts of zinc oxide nanoparticle (ZNP) on different cancer cells have been reported. Maspin (a mammary serine protease inhibitor) as a tumor suppressor gene can inhibit tumor growth and metastasis. The expression of maspin is modulated by p53, Bcl-2 family genes, and estrogen receptor α (ER-α). This study aimed to assess the ZNP effects on maspin expression in MCF-7 cells (a breast cancer cell). Experimental groups (ZNP5, ZNP10, and ZNP20) received 5, 10, and 20 μM/mL ZNP for 48 h, respectively. 17-β-estradiol (E2) was used to evaluate the role of ER-α in the anticancer impact of ZNP. Cell viability, Annexin V, migration assay, gene expression, and western blotting methods were applied to evaluate ZNP effects on the MCF-7 cells. ZNP at the concentrations of 10 and 20 μM/mL could significantly decrease the viability and migration rate, and significantly increase apoptosis percentage in the MCF-7 cells. ZNP significantly enhanced mRNA expression and protein level of maspin in MCF-7 cells in a concentration-dependent way. ZNP concentration-dependently elevated mRNA expression and protein level of p53 and Bax while reduced the expression of Bcl-2 and ER-α. E2 promoted cancer cell growth by enhancing survival and migration rates. E2 treatment reduced mRNA expression and protein level of maspin and p53, and elevated Bcl-2 expression. ZNP considerably changed these events induced by E2 in the MCF-7 cells. It is concluded that the maspin overexpression is one of the toxic mechanisms of the ZNP on the ER-α-positive breast cancer cells, and can suppress the migration of these cells.
... The injection of AVO retained the fertility percentage and correct the damage that caused by CdCl 2 , to its normal compared to the control fertility percentage. L-arginine supplementation significantly improved sperm motility without any side effects 45,46 . ...
... As it mention above that the L-arginine has is the main source of NO. Based on this, it can be postulated that L-arginine protects spermatozoa against lipid peroxidation through increased NO production 45 . Nitric oxide has been shown to abolish free radical anions 47 . ...
The present study aimed to investigate the effect of new compound L-arginine derivative (AVO) alone or in combination with cadmium chloride on the reproductive efficiency in male rats. For these experiment 40 adult male rats and 16 adult female rats, the male were divided in to 4 groups (10 rats each for each group); Group (1): was daily received normal saline by i.p injection and served as a control. Group (2) was daily received AVO only at 72 mg/kg B.W. by ip injection. Group (3) was daily administered CdCl 2 at a dose of 225 mg/kg B.W. by i.p injection. Group (3) was daily administered of CdCl 2 at a dose of 225 mg/kg B.W. by i.p injection and after one hour of CdCl 2 administration the treated rats given the new compound AVO at a dose of 72 mg/kg B.W. by i.p injection. After 28 days 8 of each group of male were sacrificed for biochemical study of reproductive hormones (FSH, LH, and Testosterone), while other 2 male of each groups were mating with 4 females. This experiment is lasted for 21 days, the mating duration was 10 days. One male were mate with two females, the females are separated in individual cages till the parturition once the female's rats are given birth, and the number of letters are calculated. The fertility percent are documented. The obtained results indicated that cadmium chloride possesses a deleterious effect on reproductive system, induce oxidative damage, histological changes of testes, and cause clear changes on the sexual hormone. The administration of AVO with cadmium chloride is relived the hazard effects of cadmium chloride, it improved, sexual hormones includes FSH, LH and testosterone, with ameliorating the histological changes in the testes, in-addition to positive effect of AVO on the fertility.
