Cadmium-induced decrement of the LH receptor expression and cAMP levels in the testis of rats

Gunnarsson, David; Nordberg, Gunnar F.; Lundgren, Per; Selstam, Gunnar

doi:10.1016/s0300-483x(02)00440-7

Cited by 72 publications

(40 citation statements)

References 11 publications

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“…As for the LHR gene among the genes we tested, Gunnarsson et al have already reported the decrement of its expression in mature rats administered at a dose of 10 µmol/kg but not 5 µmol/kg, 12) identical to our present results. However, they did not make mention of the association between this decrement and the testicular damage.…”

Section: Resultssupporting

confidence: 82%

“…The genes examined were LHR for Leydig cells, 16) the follicle-stimulating hormone receptor (FSHR) for Sertoli cells, 17) testisspecific histone 2B (TH2B) for spermatocytes, 18,19) and transition protein 1 (TP1) 19,20) and TP2 19,21) for round spermatids. The decrement of the LHR gene expression has already been reported in the testis of rats administered with Cd, 12) while the expressional changes of the other genes have not yet been reported.…”

Section: Introductionmentioning

confidence: 96%

“…Changes in the expression of some testicular genes such as p53, 10,11) c-jun, 11) luteinizing hormone receptor (LHR), 12) heme oxygenase-1, 13) and glyceraldehyde-3-phosphatedehydrogenase (GAPDH) 14) during the development of Cd-induced testicular necrosis have already been reported. In addition, the cDNA microarray assay was performed to determine the testicular profiles of gene expression in mice administered with C 2009 The Pharmaceutical Society of Japan Cd at a non-toxic dose.…”

Section: Introductionmentioning

confidence: 99%

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Decreased Gene Expression of Testicular Cell-Specific Proteins in Cadmium-Induced Acute Testicular Toxicity

Nemoto

Miyajima

Hara

et al. 2009

JOURNAL OF HEALTH SCIENCE

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Cadmium salts induce severe acute testicular necrosis in rodents. We assessed the expression levels of the genes encoding the follicle-stimulating hormone receptor, luteinizing hormone receptor, testisspecific histone 2B, and transition proteins 1 and 2, which are preferentially expressed in Sertoli cells, Leydig cells, spermatocytes, and spermatids, respectively, by reverse transcription (RT)-PCR using total RNA prepared from the whole testes of cadmium chloride (Cd)-administered rats. Spraque Dawley rats at 3, 7, and 12 weeks of age were singly and subcutaneously injected with Cd at doses of 1, 2.5, 5, 10, 15 or 20 µmol/kg. The expression levels of all genes tested were significantly decreased at doses of over 15 µmol/kg (3-week-old rats) or over 10 µmol/kg (7-and 12-week-old rats) 96 hr after injection. Histopathological study showed that these dosages of Cd resulted in extensive disruption of the seminiferous tubules and necrosis of testicular cells, while administration of Cd at a dose of 5 µmol/kg in 7-and 12-week-old rats resulted in only partial degeneration of seminiferous tubules and testicular cells. Therefore, their reduced gene expression is likely to serve as an indicator of Cd-induced testicular necrosis accompanied by cell death. In addition, the susceptibility to Cd-induced testicular damage and decreased gene expression was higher in mature (7-and 12-week-old) rats than in immature (3-week-old) rats.

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Section: Resultssupporting

confidence: 82%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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Decreased Gene Expression of Testicular Cell-Specific Proteins in Cadmium-Induced Acute Testicular Toxicity

Nemoto

Miyajima

Hara

et al. 2009

JOURNAL OF HEALTH SCIENCE

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“…These Cd rich foods can greatly increase cadmium concentration in the human body (Friberg et al, 1985;Vahter et al, 1996;WHO, 2000). Therefore, Cd is a wide-spread environmental pollutant, characterized by its toxicity to various organs, including kidney, liver, lung, testis, brain, bone, blood system (Gunnarsson et al, 2003;WHO, 1992). The molecular mechanisms of its toxicity are not yet well defined.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant effects of curcumin against cadmium chloride-induced oxidative stress in the blood of rats

Attia¹,

Ibrahim²,

EL-Latif³

et al. 2014

J. Pharmacognosy Phytother.

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Humans are exposed to a number of toxic elements in the environment. Cadmium, widely used in industry, is a great environmental health problem of both humans and animals. Effects of reactive oxygen species (ROS) generation have been postulated to be major contributors to cadmium-exposure related disease. The aim of this study was to investigate the effect of curcumin on oxidative stress in rats exposed to cadmium. Curcumin was administered orally (600 mg/kg body weight). After 24 days, significant increases in methemoglobin percentage (metHb%), superoxide dismutase (SOD), glutathione peroxidase (GPx) activity, malondialdehyde (MDA) concentration and hemolysis test were observed in cadmium exposed rats compared to control group (P < 0.05), while GSH concentration showed insignificant change. Curcumin treatment of cadmium exposed rats significantly lowered metHb%, while significantly increased oxyhemoglobin percentage (HbO 2 %), compared to cadmium alone group (P < 0.05). Also curcumin treatment significantly increased GPx activity of cadmium exposed rats as compared to cadmium alone group (P < 0.05). Curcumin treatment of cadmium exposed rats lowered MDA concentration and hemolysis percentage by 10 and 9%, respectively. The findings of this study suggest that curcumin elevated the GPx activity of cadmium exposed rats and had ameliorative effect on lipid peroxidation and erythrocytes hemolysis. Moreover, the results of multicomponent spectrophotometric analysis suggest that curcumin treatment of lead exposed rats lowered the levels of inactive metHb level and elevated the level of active HbO 2 . Curcumin may exert its protective actions against cadmium-induced hematotoxicity in rats possibly through its antioxidant mechanisms and may have future therapeutic relevance.

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“…Cd thus accumulates in renal tubular cells; until the synthetic capacity for metallothionein is exceeded. When the concentration of Cd in the kidney reaches a critical concentration; renal dysfunction is likely to occur; thus causing oxidative damage to tissues and cells by altering lipid peroxidation and loss of membrane functions [4][5][6][7][8][9]. Cd causes damage to several organs such as liver, kidney, lung and testes following acute intoxication, and nephrotoxicity, immunotoxicity, hepatic dysfunction, osteotoxicity and tumors on prolonging exposures [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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2015

MOJT

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Background: Cadmium is a serious environmental and occupational contaminant that may represent a serious health hazard to humans and other animals. Since cadmium cannot be degraded, the risk of environmental exposure is constantly increasing because of accumulation via the food chain. Exposure to cadmium at the cellular level can produce tissue injury and damage various organs, but the underlying mechanism is enigmatic. Methods:In order to investigate its toxicity on lipid profile and malondialdehyde concentration, thirty-two rats were exposed to 100, 200 and 300 ppm cadmium in their drinking water for six weeks while the control group received distilled water for the same period.Results: At all the concentrations, cadmium produced a significant (p<0.05) dosedependent hypocholesterolemia, hypotriglyceridemia and hypophospholipidemia in the plasma and erythrocyte respectively. Exposure to cadmium resulted in increased hepatic triacylglycerol concentration, whereas brain triacylglycerol concentrations were reduced. While cadmium induced brain phospholipidosis, a reduction in liver phospholipid concentration was observed. There was a significant (p<0.05) dose-dependent increase in the plasma, erythrocyte, brain and liver malondialdehyde concentrations corresponding to 56, 89, and 69 % at high dose of 300 ppm respectively compared to control. While positive associations were observed between plasma, liver, brain, erythrocyte malondialdehyde and organ triacylglycerol and phospholipid, negative associations were observed with liver phospholipid. Conclusion:The results showed that exposure to cadmium for 6 weeks significantly causes dose-dependently up-/-down lipid profile and increased malondialdehyde concentration in rats. Keywords:Cadmium conditions. Therefore, the purpose of this research was to study the lipid profile and MDA concentrations in the plasma, erythrocyte, brain and liver of rats induced with different doses of Cd in drinking water. Materials and Methods Animals and treatmentThirty-two adult male albino Wistar rats (bred in the Animal House of the Department of Biochemistry; Faculty of Sciences; Lagos State University; Ojo; Lagos; Nigeria) with body weight between 180 and 200g were used for the experiment. They were housed in animal stainless cages with a 12h light/dark cycle and free access to food and water for 14days prior to the experiment. The animals were randomly and equally distributed into four groups (n=8). Animals in group one were given distilled water and served as controls while rats in three other groups were given 100; 200 and 300 ppm Cd in the form of Cd-chloride in drinking water respectively for short-term exposure of six weeks. All groups were fed ad libitum with grower mash with minimal Cd level (product of Animal care; Lagos; Nigeria). Although the levels surpassed Cd levels to which humans are exposed to in water [16]; but the concentrations embodied levels of Cd that have elicited toxic effect in rats [17,18].At the end of Cd exposure; the rats were fasted overnight and ...

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Cadmium-induced decrement of the LH receptor expression and cAMP levels in the testis of rats

Cited by 72 publications

References 11 publications

Decreased Gene Expression of Testicular Cell-Specific Proteins in Cadmium-Induced Acute Testicular Toxicity

Decreased Gene Expression of Testicular Cell-Specific Proteins in Cadmium-Induced Acute Testicular Toxicity

Antioxidant effects of curcumin against cadmium chloride-induced oxidative stress in the blood of rats

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