Cadmium-induced Damage Research Articles

Epigallocatechin gallate protects MC3T3-E1 cells from cadmium-induced apoptosis and dysfunction via modulating PI3K/AKT/mTOR and Nrf2/HO-1 pathways.

Epigallocatechin gallate (EGCG), an active constituent of tea, is recognized for its anticancer and anti-inflammatory properties. However, the specific mechanism by which EGCG protects osteoblasts from cadmium-induced damage remains incompletely understood. Here, the action of EGCG was investigated by exposing MC3T3-E1 osteoblasts to EGCG and CdCl2 and examining their growth, apoptosis, and differentiation. It was found that EGCG promoted the viability of cadmium-exposed MC3T3-E1 cells, mitigated apoptosis, and promoted both maturation and mineralization. Additionally, CdCl2 has been reported to inhibit both the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and nuclear factor erythroid 2-related factor 2/heme oxygenase-1(Nrf2/HO-1) signaling pathways. EGCG treatment attenuated cadmium-induced apoptosis in osteoblasts and restored their function by upregulating both signaling pathways. The findings provide compelling evidence for EGCG's role in attenuating cadmium-induced osteoblast apoptosis and dysfunction through activating the PI3K/AKT/mTOR and Nrf2/HO-1 pathways. This suggests the potential of using EGCG for treating cadmium-induced osteoblast dysfunction.

Potential Protective Effect of Selenium-Enriched Lactobacillus plantarum on Cadmium-Induced Liver Injury in Mice.

Cadmium (Cd) is a prevalent environmental contaminant that poses a potential hazard to the health of both humans and animals. In this study, biosynthesized selenium-enriched Lactobacillus plantarum and selenium nanoparticles (SeNPs) were developed and evaluated for their protective effects against Cd-induced hepatic injury in mice through oral administration for 4 weeks. Cadmium exposure resulted in severe impairment of liver function, as evidenced by increased levels of serum markers of liver injury and, oxidative stress and significant damage to liver tissue, and a notable decrease in the diversity of the intestinal microbiota. Oral administration of Se-enriched L. plantarum (LS) reduced cadmium accumulation in the liver by 49.5% and, restored other cadmium-induced damage markers to normal levels. A comparison of the effects with those of L. plantarum (L) and SeNPs isolated from LS revealed that LS could more effectively alleviate hepatic oxidative stress and reduce the intrahepatic inflammatory responses of the liver, further protecting against cadmium-induced liver injury. These findings suggest that the development of LS may be effective at protecting the liver and intestinal tract from cadmium-induced damage.

Vitamin D In Modulating Liver And Kidney Functions Following Cadmium Exposure In Vivo

Background: Cadmium is known to affect liver and kidney function due to its toxicity detrimentally. Vitamin D reportedly mitigates cadmium-induced damage in various organs, yet its specific role in liver and kidney protection requires validation. Method: 24 male rats received cadmium chloride (CD) and nutritional vitamin D via intramuscular administration for 6 weeks. Liver and kidney function were assessed through ALT, AST, ALP, CRE, UA levels, and total protein concentration. Result: Groups A and B exhibited significant elevation (P<0.001) in ALT, AST, ALP, CRE, and UA levels compared to controls for 4 weeks, indicating cadmium-induced impairment. However, these markers significantly decreased after 6 weeks of vitamin D3 treatment, signifying improved liver and kidney function. Both groups showed increased TP levels compared to controls. Conclusion: Vitamin D mitigates liver and kidney damage induced by cadmium in adult male rats. The study highlights the protective effects of vitamin D against cadmium toxicity, potentially preserving organ function under toxin-induced stress.

Cadmium Toxicity in the Seminal Vesicles and Lipid Profile of Wistar Rats: Can Uvaria chamae Ameliorate the Effect?

This research investigated the capacity of Uvaria chamae in alleviating cadmium-induced toxicity in the seminal vesicles and lipid profile of Wistar rats, addressing a critical gap in current knowledge. Cadmium, a hazardous heavy metal, poses substantial risks to male reproductive health. Conducted with 25 Wistar rats under controlled conditions, the study involved local sourcing of Uvaria chamae, extracting its bioative ingredients through alcohol maceration. Dosages for cadmium and the extract were meticulously determined for five experimental groups including the control group, with rats acclimatized for two weeks before a 28-day experiment. Seminal vesicle underwent detailed processing, and histological analysis, including dehydration, clearing, infiltration, embedding, sectioning, staining using hematoxylin/eosin and microscopic examination. Statistical analysis employed one-way ANOVA through GraphPad Prism (version 8.0.2), ensuring a concise and accurate data interpretation approach. Histological examinations revealed cadmium-induced damage, including epithelial degeneration and altered luminal structures etc. These structural changes were mitigated by Uvaria chamae in a dose-dependent manner. The study also assessed the impact of cadmium on lipid profiles, showing adverse changes, but counteracted by Uvaria chamae, signifying its role in preserving lipid homoeostasis. The findings underscore reproductive health risks from cadmium exposure and highlight Uvaria chamae's therapeutic potential, which is attributed to its antioxidant and anti-inflammatory properties. This research offers valuable scientific insights on the plant and thereby urging further investigations into molecular mechanisms, clinical trials, public awareness, environmental regulations, and nutritional guidance for enhanced reproductive health amid cadmium exposure.

Preparation of pectin from fingered citron peel and its protective effect on cadmium-induced liver and kidney damage in mice

Citrus pectin has been proved for its ability to bind heavy metals from industrial wastewater. However, few studies have investigated the detoxification effect of citrus pectin on cadmium-induced damage through in vivo experiments. In this study, pectin was extracted from fingered citron peel and subjected to pH-temperature modification, and successful modification of pectin's molecular structure was confirmed by a decrease in the degree of esterification and the increase in the content of free carboxylate groups in the structure. In vitro studies suggested that the modified fingered citron peel pectin (mFCPP) showed higher cadmium removal ability compared to unmodified fingered citron peel pectin (FCPP). A 20-week study in cadmium-exposed mice suggested significant improvement in liver and kidney function with co-treatment of pectin. Co-treatment with FCPP or mFCPP ameliorated the cadmium-induced cell death and oxidative damage in the liver and kidney. Moreover, the study demonstrated that both FCPP and mFCPP were impermeable through the intestinal wall, suggesting their binding with the cadmium ions in the gastrointestinal tract, thus preventing cadmium ions absorption and entry into the systemic circulation.

Protective Effect of Astragaloside IV against Cadmium-Induced Damage on Mouse Renal Podocytes (MPC5).

In this study, we investigated the protective effect of Astragaloside IV (Ast) on mouse podocytes and its possible mechanism of action by constructing a cadmium-induced mouse renal podocytes model. We investigated the effects of cadmium (Cd) toxicity on cell number, morphology, the mitochondrial status of subcellular organelles, protein and gene levels, and the protective effects of Ast by constructing a model of Cd-induced damage to mouse renal podocytes (MPC5) and giving Ast protection at the same time. The results showed that exposure of MPC5 cells to CdCl2 culture medium containing 6.25 μM concentration acted with low cell mortality, but the mortality of MPC5 cells increased with the prolongation of cadmium exposure time. Given Ast, the death rate in the low dose group (12.5 μM) was significantly reduced, while the death rate in the medium dose group (25 μM) was extremely significantly reduced. In comparison to the control group, the Cd-exposed group exhibited a significant increase of 166.7% in malondialdehyde (MDA) content and a significant decrease of 17.1% in SOD activity. The mitochondrial membrane potential was also reduced to varying degrees. However, in the Ast-protected group compared to the Cd-exposed group, the MDA content significantly decreased by 20.8%, the SOD activity decreased by 7.14%, and the mitochondrial membrane potential showed a significant increase. Fluorescence staining of mitochondrial membrane potential indicated that Cd exposure caused mitochondrial apoptosis. In the 12-h cadmium-exposed group, the protein expression of Nephrin in mice significantly decreased by 33.4%. However, the expression of the Desmin protein significantly increased by 67.8%, and the expression of the autophagy protein LC3-II significantly increased by 55.5%. Meanwhile, the expression of PINK1, a mitochondrial autophagy pathway protein, was significantly increased in the 12 h and 24 h cadmium exposure groups. The mRNA level of PINK1 was significantly increased, and that of Parkin was decreased in the 48 h cadmium exposure group. Compared to the Cd-exposed group, the Ast group showed more significant improvements in the expression of podocyte structure, functional proteins, and mitochondrial autophagy pathway proteins. The immunological assay of mitochondrial autophagic pathway proteins further indicated that Cd-induced damage to MPC5 cells might be associated with the dysregulation of mitochondrial autophagy.

Naringenin mitigates cadmium-induced cell death, oxidative stress, mitochondrial dysfunction, and inflammation in KGN cells by regulating the expression of sirtuin-1

The objective of this study was to examine the potential protective role of naringenin against the harmful effects induced by cadmium in KGN cell line. Cell viability was evaluated by cell counting kit-8 assay. Caspase-3/-9 activities were determined by caspase-3/-9 activity assay kits, respectively. Intracellular reactive oxygen species (ROS) level was detected by ROS-Glo™ H2O2 Assay, antioxidant capacity was determined by a total antioxidant capacity assay kit. Mitochondrial membrane potential (MMP), ATP level, and ATP synthase activity were determined by JC-1, ATP assay kit, and ATP synthase activity assay kit, respectively. The mRNA expression was determined by qRT-PCR. Cadmium reduced cell viability and increased caspase-3/-9 activities in a concentration-dependent manner. Naringenin improved cell viability and reduced caspase-3/-9 activities in cadmium-stimulated KGN cells in a concentration-dependent manner. Cadmium diminished the antioxidant capacity, increased ROS production, and induced mitochondrial dysfunction in KGN cells. These effects were ameliorated by naringenin treatment in a concentration-dependent manner. Furthermore, naringenin reduced the levels of pro-inflammatory cytokines in KGN cells exposed to cadmium. SIRT1 knockdown downregulated its expression in KGN cells and compromised the protective effects of naringenin on cell viability and caspase-3/-9 activities in cadmium-stimulated KGN cells. Naringenin prevented the reduction of MMP, ATP levels, and ATP synthase activity in cadmium-stimulated KGN cells in a concentration-dependent manner. However, these protective effects were significantly reversed by SIRT1 knockdown. In conclusion, this study suggests that naringenin protects against cadmium-induced damage by regulating oxidative stress, mitochondrial function, and inflammation in KGN cells, with SIRT1 playing a potential mediating role.

Does L-Carnitine Prevent Cadmium-Induced Damage in Gastrointestinal Contractility and Histological Changes in Prepubertal Rat

Does L-Carnitine Prevent Cadmium-Induced Damage in Gastrointestinal Contractility and Histological Changes in Prepubertal Rat

Physiological and biochemical mechanisms of brassinosteroid in improving anti-cadmium stress ability of Panax notoginseng

In this study, the effect of brassinosteroid(BR) on the physiological and biochemical conditions of 2-year-old Panax notoginseng under the cadmium stress was investigated by the pot experiments. The results showed that cadmium treatment at 10 mg·kg~(-1) inhibited the root viability of P. notoginseng, significantly increased the content of H_2O_2 and MDA in the leaves and roots of P. noto-ginseng, caused oxidative damage of P. notoginseng, and reduced the activities of SOD and CAT. Cadmium stress reduced the chlorophyll content of P. notoginseng, increased leaf F_o, reduced F_m, F_v/F_m, and PIABS, and damaged the photosynthesis system of P. notoginseng. Cadmium treatment increased the soluble sugar content of P. notoginseng leaves and roots, inhibited the synthesis of soluble proteins, reduced the fresh weight and dry weight, and inhibited the growth of P. notoginseng. External spray application of 0.1 mg·L~(-1) BR reduced the H_2O_2 and MDA content in P. notoginseng leaves and roots under the cadmium stress, alleviated cadmium-induced oxidative damage to P. notoginseng, improved the antioxidant enzyme activity and root activity of P. notoginseng, increased the content of chlorophyll, reduced the F_o of P. notoginseng leaves, increased F_m, F_v/F_m, and PIABS, alleviated the cadmium-induced damage to the photosynthesis system, and improved the synthesis ability of soluble proteins. In summary, BR can enhance the anti-cadmium stress ability of P. notoginseng by regulating the antioxidant enzyme system and photosynthesis system of P. notoginseng under the cadmium stress. In the context of 0.1 mg·L~(-1) BR, P. notoginseng can better absorb and utilize light energy and synthesize more nutrients, which is more suitable for the growth and development of P. notoginseng.

Zinc Chloride Can Mitigate the Alterations in Metallothionein and Some Apoptotic Proteins Induced by Cadmium Chloride in Mice Hepatocytes: A Histological and Immunohistochemical Study.

The heavy metal cadmium is extremely harmful to both humans and animals. Zinc supplementation protects the biological system and reduces cadmium-induced toxicity. This study aimed to determine whether zinc chloride (ZnCl2) could protect male mice with the damaged liver induced by cadmium chloride (CdCl2). The protective role of zinc chloride and expression of the metallothionein (MT), Ki-67, and Bcl-2 apoptotic proteins in hepatocytes were studied after subchronic exposure of mice to cadmium chloride for 21 days. Thirty male mice were randomly categorized into 6 groups (5 mice/group) as follows: a control group that did not receive any treatment, a group given ZnCl2 at 10 mg/kg alone, and two groups received ZnCl2 (10 mg/kg) in combination with CdCl2 at two concentrations (1.5 and 3 mg/kg), while the last two groups received CdCl2 alone at 1.5 and 3 mg/kg, respectively. Immunohistochemical examination revealed a decrease in Ki-67 expression in Kupffer and endothelial cells, which reflected cell proliferation downregulation accompanied by MT increased expression. However, the Bcl-2 was ameliorated and reduced to demonstrate an enhanced rate of necrosis rather than apoptosis. Furthermore, histopathological results showed significant alteration such as hepatocytes with a pyknotic nucleus, infiltration of inflammatory cells around the central vein, and the presence of many binucleated hepatocytes. Zinc chloride treatment resulted in histological and morphological improvements that were average in the expression of apoptosis proteins modifications induced by cadmium. Our findings revealed that the positive effects of zinc might be linked to the high metallothionein expression and enhanced cell proliferation. Furthermore, at low-dose exposure, cadmium-induced damage to cells could be more closely related to necrosis rather than apoptosis.

Indispensable role of melatonin, a scavenger of reactive oxygen species (ROS), in the protective effect of Akkermansia muciniphila in cadmium-induced intestinal mucosal damage.

The gastrointestinal tract is the main target of cadmium toxicity. However, whether Akkermansia muciniphila (A. muciniphila), which has been reported to be the next generation of promising probiotics, can alleviate cadmium-induced intestinal damage has not been investigated. In this study, we found that compared to the cadmium exposure group, mice gavaged with A. muciniphila showed less severe intestinal mucosal damage, with improved bodyweight, colon length, a decline in inflammation, and significantly increased glutathione and goblet cell numbers. Meanwhile, melatonin was interestingly found to be strikingly increased after A. muciniphila treatment. We then demonstrated that melatonin also could ameliorate the intestinal mucosal damage caused by cadmium through scavenging reactive oxygen species (ROS) and increasing the number of goblet cells. Furthermore, mice treated with inhibitors had a low level of melatonin and could not reproduce the beneficial effects of the A. muciniphila. Our results implied that the regulation of melatonin production by A. muciniphila is associated with an increase in enterochromaffin cells number, which determine melatonin secretion. This study indicated that the A. muciniphila-melatonin axis reduces cadmium-induced damage by increasing the goblet cells and scavenging the ROS, which may guide the prevention of the toxic effects of heavy metals.

Bifunctional core-shell structure NaA zeolite@mesoporous-silica/curcumin nanocomplexes for removing heavy metals and reduction of Cadmium-induced damage

Heavy metals had been reported to bioaccumulate in many organs and adversely affect the functions of these organs. Therefore, it was of great significance to develop bifunctional drug carrier, which could remove heavy metals and load curcumin with multiple protective properties. Newly designed drug carrier combining a core of NaA zeolite and a mesoporous silica (MS) shell has been developed, which the core is used to remove heavy metals, the outer shell loads drugs, and explore the dual functions. In this work, Curcumin-loaded on an amino modified NaA@MS-0.2 (NaA@MS-0.2-N-Cur) are 220 nm sized and have a mesoporous silica shell of 30 nm thickness. The cumulative drug release from NaA@MS-0.2-N-Cur were 14.1 and 43.0% in pH 7.4 and pH 1.2 PBS. NaA@MS-0.2-N-Cur released in 100 mL of pH 1.2 PBS containing 100 mg/L Cd2+, the cumulative drug release rate was 43.9%, the sorption rate of Cd2+ was 79.7%, and the sorption capacity of Cd2+ was 109.5 mg/g. Taken together, these results suggested that core-shell structure nanocomplexes are bifunctional and its cumulative drug release rate increased in pH 1.2 PBS. And this drug carrier has great potential for protecting the body from damage for heavy metal.

The Influence of Interaction between Cadmium with 17β-Estradiol, 2-Methoxyestradiol and 16α-Hydroxyestrone on Viability and p-Glycoprotein in Ovarian Cancer Cell Line.

Occupational and environmental exposure to xenoestrogens, a subgroup of endocrine disruptors (EDCs), can affect the endocrine system and increase the risk of cancer, primarily the hormone-dependent kind. This type of cancer includes ovarian cancer, which is the leading cause of death from gynecological tumors. The aim of this study was to assess the role of 17β-estradiol and its metabolites: 2-MeOE2, 16α-OHE1 in exposure to the metalloestrogen cadmium. The effect of interactions of cadmium with estrogens on the viability of cells in malignant ovarian cancer cells SKOV-3 was investigated, both in simultaneous action and in the pre-incubation model. There are no known interactions between estrogens and cadmium in ovarian cancer cells. Due to the frequent occurrence of multidrug resistance (MDR) in ovarian cancer, the effects of estrogens and cadmium on MDR in SKOV-3, measured as P-glycoprotein (P-gp), were assessed. An interaction study showed that E2 had an antagonistic effect on cadmium-induced cell damage, while 2-MeOE2 showed less of a protective effect in combination with CdCl2 than E2. There were two types of interaction: toxic synergism and beneficial antagonism. E2 and cadmium increased P-gp expression in SKOV-3 cells, while 2-MeOE2 decreased P-gp expression to a potentially beneficial effect on MDR prevention. The obtained results constitute an interesting starting point for further research in the field of interactions between estrogens and xenoestrogens in ovarian cancer.

Effect of quercetin and curcumin in rats sub-acutely exposed to cadmium chloride: haemato-biochemical changes, oxidative stress parameters and histopathological changes in intestine, liver and kidney of rats

Quercetin is a flavonoid mostly found in fruits and vegetables. Curcumin is the main natural polyphenol found in the rhizome of Curcuma longa and in others Curcuma spp.. Individually, quercetin and curcumin had shown to have various pharmacological properties. The increasing level of cadmium in the environment is alarming as cadmium affects the antioxidant defense system with ability to persist in the body for long time. The bioaccumulation of cadmium is well-known, which is dangerous for the health of human and animals after continuous exposure to it. The present experiment was carried out to evaluate the ameliorating effect of quercetin (50 mg/kg daily orally for 28 days) and curcumin (100 mg/kg daily orally for 28 days) alone and in combination of both against cadmium-induced (100 ppm in water for 28 days) alterations in biochemical markers and histological changes in intestine, liver and kidney of rats. Body weight gain in rats of toxicity group during the 4th week of study period was significantly affected by the cadmium. Cadmium exposure significantly increased the levels of AST, ALT, ALP, bilirubin and glucose in serum along with higher level of MDA in intestine, liver and kidney of rats. The administration of quercetin and curcumin in combination as compared to individual treatment along with cadmium exposure had shown significantly lower levels of above parameters. Various histological changes were noticed in intestine, liver and kidney of rats following exposure to cadmium which were improved in rats treated with individual or combined treatment of quercetin and curcumin. Quercetin alone had shown the ameliorating effect against cadmium-induced alteration in kidney of rats. While, combination of quercetin and curcumin has been found to protect the intestine and liver from cadmium-induced damage following sub-acute exposure in rats. However, further study is needed to explore the mechanism of protective effect of the quercetin and curcumin against cadmiuminduced changes in intestine, liver and kidney.

Quercetin Protects Human Thyroid Cells against Cadmium Toxicity.

Various natural compounds have been successfully tested for preventing or counteracting the toxic effects of exposure to heavy metals. In this study, we analyzed the effects of cadmium chloride (CdCl2) on immortalized, non-tumorigenic thyroid cells Nthy-ori-3-1. We investigated the molecular mechanism underlying its toxic action as well as the potential protective effect of quercetin against CdCl2-induced damage. CdCl2 suppressed cell growth in a dose- and time-dependent manner (IC50 value ~10 μM) associated with a decrease in levels of phospho-ERK. In addition, CdCl2 elicited an increase in reactive oxygen species (ROS) production and lipid peroxidation. A significant increase in GRP78, an endoplasmic reticulum (ER) stress-related protein, was also observed. Supplementation of quercetin counteracted the growth-inhibiting action of CdCl2 by recovering ERK protein phosphorylation levels, attenuating ROS overproduction, decreasing MDA content and reducing the expression of GRP78 in cells exposed to CdCl2. Thus, in addition to revealing the molecular effects involved in cadmium-induced toxicity, the present study demonstrated, for the first time, a protective effect of quercetin against cadmium-induced damages to normal thyroid cells.

Histomorphological Profile of Liver and Kidney Tissues of Albino Wistar Rats Following Exposure to Cadmium-Induced Damage and Ascorbic Acid Supplementation

Introduction: Cadmium is a common heavy metal toxicant that can cause diverse tissue toxicities and pathologies. Conversely, ascorbic acid is a natural anti-oxidant that can ameliorate cytotoxic effects of tissue toxicants. In this study, the objective was to assess the histomorphological profile of liver and kidney tissues of albino Wistar rats after exposure to cadmium-induced damage and ascorbic acid supplementation. Subjects and Methods: 24 animals were divided into four groups (1-4) comprising of six animals each (n=6). Normal control group 1 was given distilled water, test control group 2 given 5 mg/kg Cadmium chloride and test groups 3 and 4 given 5 mg/kg Cadmium chloride + 100 mg/kg ascorbic acid and 5 mg/kg + 200 mg/kg ascorbic acid respectively. The route of the 21 days administration was oral. Thereafter, the liver and kidney of experimental animals were harvested, weighed and processed. Results: Only the test control group 2 showed significant (p < 0.05) reduction in mean organ weight compared to normal control group 1. Similarly, only the test control group 2 animals showed significant alterations in the liver and kidney histomorphological profile compared to normal control group 1. Conclusion: The ascorbic acid exhibited prominent ameliorative effect against damaging effect of cadmium exposure leading to relative reparation of liver and kidney histomorphology in albino Wistar rats.

Selenium supplementation alleviates cadmium-induced damages in tall fescue through modulating antioxidant system, photosynthesis efficiency, and gene expression.

Selenium (Se) is beneficial for plant growth under different stressful conditions. In this study, we investigated the protective effects of Se supply from Cd-induced damages in tall fescue under Cd stress. Tall fescue seedlings (40days old) were treated with Cd (30mg/L, as CdSO4·8/3 H2O) and Se (0.1mg/L, as Na2SeO3) individually and in combination using 1/2 Hoagland's solution system for 7days. Various physiological parameters, photosynthetic behaviors, and gene expressions were measured. The results showed that Cd-stressed plants displayed obvious toxicity symptoms such as leaf yellowing, decreasing plant height, and root length. Cd stress significantly increased the malondialdehyde (MDA) content and electrolyte leakage (EL), and remarkably reduced the chlorophyll and soluble protein content, antioxidant enzyme activities, and photosynthetic efficiency. Cd stress significantly inhibited the expression of two photosynthesis-related genes (psbB and psbC), but not psbA. In addition, it significantly inhibited the expression of antioxidant system-related genes such as ChlCu/ZnSOD, CytCu/ZnSOD, GPX, and pAPX, but significantly increased the expression of GR. However, Se improved the overall physiological and photosynthetic behaviors of Cd-stressed plants. Se significantly enhanced the chlorophyll and soluble protein content and CAT and SOD activities, but decreased MDA contents, EL, and Cd content and translocation in tall fescue under Cd stress. Furthermore, under Cd stress, Se increased the expression of psbA, psbB psbC, ChlCu/ZnSOD, CytCu/ZnSOD, GPx, and PAPx. The result suggests that Se alleviated the deleterious effects of Cd and improved Cd resistance in tall fescue through upregulating the antioxidant system, photosynthesis activities, and gene expressions.

Can L-carnitine prevent Cadmium-Induced Damage of the Developing Hippocampus?

Background: Cadmium is used in everyday life aspects. Hippocampus plays important role in the memory process and could be affected by cadmium exposure. L-carnitine is antioxidant, its role in neuroprotection is still not known. Aim of work: To assess effects of pre- and postnatal cadmium exposures on structure of principle cells (pyramidal and granular) of hippocampus in albino rats, and the potential role of L-carnitine. Material and methods: Pregnant female albino rats were used and divided into two major groups: I- Pregnancy and II- Lactation, each was further equally subdivided into 4 subgroups: Group Ia- Control. Group Ib- received cadmium from pregnancy day (PD)10 until delivery. Group Ic- received L-carnitine from PD7 until delivery. Group Id- received both L-carnitine from PD7 + cadmium from PD10 until delivery. Group IIa- Control. Group IIb- received cadmium from day 0-21. Group IIc- received L-carnitine from day 0-21. Group IId- received both L-carnitine+cadmium from day 0-21. Cadmium chloride was given orally by gastric lavage 4 mg/kg bodyweight/day. L-carnitine dose was given as 200 mg/kg/day orally by gastric lavage. The hippocampal specimens were collected from twelve male offspring of both age subgroups (newborn and 21 day old; 96 rats total) and were processed for light, electron microscopy and morphometry. Results: In cadmium received rats principle cells showed degenerative changes as pyknosis, cytoplasmic vacuoles, damaged mitochondria, indentation of nuclear membrane, and the morphometric data showed highly significant reduction in principle cells number and decreased principle cell layer thickness as compared to control. In cadmium+L-carnitine received rats the principle cells showed a very few swollen cells with little vacuoles, mildly dilated rough endoplasmic reticulum, and the morphometric results were improved approaching those of the control. Conclusion: cadmium damaged principle cells of dentate gyrus, CA3 and CA1 fields of the rat hippocampus. L-carnitine reduced the cadmium-induced neuronal damage.

Cadmium induced damage in Wistar rats, ameliorative potentials of progesterone

Asides the increased human exposure to Cadmium containing products; the adverse effects of Cadmium on human health is further exacerbated by its toxicity at low dosage, long biologic half-life and low rate of excretion from the body.This study investigated the protective potential of progesterone on cadmium-induced damage in Wistar rats.Adult male Wistar rats received CdCl2 once daily for 21 days. Progesterone was given 30 min. after administration of CdCl2 while 3 other groups were given distilled water, CdCl2 and progesterone alone. Blood samples were collected from the animals for the determination of liver function and antioxidant status while the liver, kidney, cerebellar and hippocampal tissues were excised and fixed in Neutral buffered formalin for histopathological studies.While Cadmium caused changes in liver function parameters which were indicative of oxidative stress, pre-treatment with progesterone caused restoration to values which were non-significant to the control. Similar findings were made for G6PD, GSH, SOD, CAT and MDA. Histopathology revealed tissue damage in the Cd treated group; this was attenuated by prior treatment with progesterone.Progesterone ameliorated the free radical induced oxidative stress and tissue injury arising from exposure to Cadmium; attention should be given to its antioxidant role in Cadmium toxicity.

Protective Effect of Agaricus blazei Polysaccharide Against Cadmium-Induced Damage on the Testis of Chicken.

Cadmium (Cd) exposure can cause reproductive toxicity through oxidative stress and inflammatory response. A polysaccharide extract of the edible mushroom Agaricus blazei Murill has been isolated and exhibits antioxidant activity and immunoregulatory effect. The aim of this study was to investigate the protective role of Agaricus blazei polysaccharide (ABP) against Cd-induced damage in chicken testis through enhancing antioxidant activity and alleviating inflammatory response. One hundred twenty healthy 7-day-old Hy-Line male chickens (Harbin, China) were randomly divided into four groups, and each group consisted of 30 chickens: Normal control was fed daily with full feed and 0.2mL distilled water per day via oral gavage; Cd-treated group was fed daily with full feed that contained 140mg/kg CdCl2 and 0.2mL distilled water per day by gavage; Polysaccharide-treated group was fed daily with full feed with 0.2mL ABP(30mg/ml) solution per day via oral gavage; Cd/polysaccharide-treated group was fed daily with full feed containing 140mg/kg CdCl2 and 0.2mL ABP(30mg/ml) solution per day by gavage. On the 20, 40, and 60days, the testis was immediately removed. The contents of Cd in the testis, activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), malondialdehyde (MDA) production, messenger RNA (m RNA) levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), protein expressions of heat shock proteins (HSPs) (HSP60, HSP70, and HSP90), and the histopathological changes of the testis were determined. The results indicated that ABP improved Cd-caused testicular tissue damage by increasing the SOD and GSH-Px activities: decreasing the Cd accumulation and MDA content, mRNA levels of TNF-α, IL-1β, and IL-6, and protein expressions of HSP60, HSP70, and HSP90. Results suggest that ABP for the mitigation of damage induced by cadmium in chicken testis through enhancing antioxidant activity and alleviating Inflammatory response.