Spirulina platensis shields the submandibular gland from cadmium toxicity by bolstering antioxidant defenses and maintaining its structural integrity.

Cadmium (Cd), an element categorized as a non-essential transitional metal, has potential hazards to the health of both human beings and animals. Spirulina platensis (SP), a type of blue-green algae, possesses a high concentration of essential antioxidants. The present study aimed to explore the possible defensive role of SP against Cd-induced submandibular gland injury in rats by assessment of biomarkers related to both oxidative stress and inflammatory processes, which were further explored through histopathological examination of submandibular gland tissue. Consequently, the study included 32 mature rats, subdivided into four different groups as follows: control, SP, Cadmium chloride (CdCl2), and CdCl2/SP. The duration of the study was 24days. The results revealed that CdCl2 induced submandibular gland injury as shown by the oxidant/antioxidant imbalance and increased inflammatory reactions, in addition to, histopathological changes and overexpression of BAX immunostaining. Concurrent SP administration to CdCl2-treated rats significantly improved all these effects. We concluded that concurrent SP supplement improved the submandibular gland injury provoked by CdCl2.

Protective effect of naringenin on cadmium chloride-induced renal injury via alleviating oxidative stress, endoplasmic reticulum stress, and autophagy in chickens.

Cadmium (Cd) is a highly hazardous toxic substance that can cause serious harm to animals. Previous studies have indicated that cadmium chloride (CdCl2) can damage organs, such as the liver, ovaries, and testicles. Naringenin (Nar) represents a flavonoid with various properties that promote the alleviation of Cd-induced damage. In this experiment, 60 chickens were divided into the control group, 150 mg/kg CdCl2 treatment group, 250 mg/kg Nar treatment group, and 150 mg/kg CdCl2 + 250 mg/kg Nar co-treatment group, which were treated for 8 weeks. Kidney tissues samples were collected to investigate kidney function, including oxidative stress (OS), endoplasmic reticulum (ER) stress, and autophagy activity. Experimental results showed the decreased weight of chickens and increased relative weight of their kidneys after CdCl2 treatment. The increase in NAG, BUN, Cr, and UA activities, as well as the increase in MDA and GSH contents, and the decrease activities of T-AOC, SOD, and CAT in the kidney, manifested renal injury by OS in the chickens. TUNEL staining revealed that CdCl2 induced apoptosis in renal cells. CdCl2 upregulates the mRNA and protein expression levels of GRP78, PERK, eIF2α, ATF4, ATF6, CHOP, and LC3, and inhibited the mRNA and protein expression levels of P62 proteins, which leads to ER stress and autophagy. The CdCl2 + Nar co-treatment group exhibited alleviated CdCl2-induced kidney injury, OS, ER stress, and autophagy. Research has demonstrated that Nar reduces CdCl2-induced kidney injury through alleviation of OS, ER stress, and autophagy.

Mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.

An earlier study found that respiratory cadmium chloride (CdCl2) exposure caused COPD-like lung injury. This study aimed to explore whether mitochondrial dysfunction-mediated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury. Adult C57BL/6 mice were exposed to CdCl2 (10 mg/L) aerosol for six months. Beta-galactosidase-positive cells, p21 and p16 were increased in CdCl2-exposed mouse lungs. The in vitro experiments showed that γ-H2AX was elevated in CdCl2-exposed alveolar epithelial cells. The cGAS-STING pathway was activated in CdCl2-exposed alveolar epithelial cells and mouse lungs. Cxcl1, Cxcl9, Il-10, Il-1ß and Mmp2, several senescence-associated secretory phenotypes (SASP), were upregulated in CdCl2-exposed alveolar epithelial cells. Mechanistically, CdCl2 exposure caused SIRT3 reduction and mitochondrial dysfunction in mouse lungs and alveolar epithelial cells. The in vitro experiment found that Sirt3 overexpression attenuated CdCl2-induced alveolar epithelial senescence and SASP. The in vivo experiments showed that Sirt3 gene knockout exacerbated CdCl2-induced alveolar epithelial senescence, alveolar structure damage, airway inflammation and pulmonary function decline. NMN, an NAD+ precursor, attenuated CdCl2-induced alveolar epithelial senescence and SASP in mouse lungs. Moreover, NMN supplementation prevented CdCl2-induced COPD-like alveolar structure damage, epithelial-mesenchymal transition and pulmonary function decline. These results suggest that mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.

Caffeic acid attenuates memory dysfunction and restores the altered activity of cholinergic, monoaminergic and purinergic in brain of cadmium chloride exposure rats.

OBJECTIVES: This study aims to evaluate the neuroprotective effect of caffeic acid (CAF) against cadmium chloride (CdCl2) in rats via its effect on memory index as well as on altered enzymatic activity in the brain of CdCl2-induced neurotoxicity. METHODS: The experimental rats were divided into seven groups (n=6 rats per group) of healthy rats (group 1), CdCl2 -induced (CD) (3 mg/kg BW) rats (group 2), CD rats + Vitamin C (group 3), CD rats + CAF (10 and 20 mg/kg BW respectively) (group 4 & 5), and healthy rat + CAF (10 and 20 mg/kg BW respectively) (group 6 & 7). Thereafter, CdCl2 and CAF were administered orally to the experimental rats in group 2 to group 5 on daily basis for 14 days. Then, the Y-maze test was performed on the experimental rats to ascertain their memory index. RESULTS: CdCl2 administration significantly altered cognitive function, the activity of cholinesterase, monoamine oxidase, arginase, purinergic enzymes, nitric oxide (NOx), and antioxidant status of Cd rats (untreated) when compared with healthy rats. Thereafter, CD rats treated with vitamin C and CAF (10 and 20 mg/kg BW) respectively exhibited an improved cognitive function, and the observed altered activity of cholinesterase, monoamine oxidase, arginase, purinergic were restored when compared with untreated CD rats. Also, the level of brain NOx and antioxidant status were significantly (p<0.05) enhanced when compared with untreated CD rats. In the same vein, CAF administration offers neuro-protective effect in healthy rats vis-à-vis improved cognitive function, reduction in the activity of some enzymes linked to the progression of cognitive dysfunction, and improved antioxidant status when compared to healthy rats devoid of CAF. CONCLUSIONS: This study demonstrated the neuroprotective effect of CAF against CdCl2 exposure and in healthy rats.

Influence of titanium dioxide nanoparticles and/or cadmium chloride oral exposure on testicular morphology, oxidative stress, and apoptosis in rats: Ameliorative role of co-enzyme Q10.

Background and objectives: Little is known about the implications of titanium dioxide nanoparticles (TiO2NPs) and cadmium chloride (Cd) co-exposure on the male reproductive system in mammals. As a result, this study researched the effects of oral TiO2NPs and/or Cd exposure on male reproduction and testicular functions. Additionally, a mitigation trial with co-enzyme Q10 (CoQ10) has also been conducted. Methods: In a 60-day experiment, seven experimental groups, each containing 10 male Sprague Dawley rats, were orally given distilled water (control), corn oil (vehicle control), CoQ10 (10 mg/kg b.wt), TiO2NPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TiO2NPs + Cd, and TiO2NPs + Cd + CoQ10. Then, sperm quality, male sex hormones, oxidative stress indications, Ti and Cd testicular residues, testes and accessory gland architecture, and apoptotic and inflammatory markers in rat testes were assessed. Results: TiO2NPs and/or Cd exposure negatively impacted body weight, weight gain, testicular weights, semen quality, serum reproductive hormones, oxidative stress parameters, and Caspase-3 and tumor necrosis factor (TNF-α) immunoreactions. Histopathological changes were recorded in testicular, seminal vesicle, and prostatic tissues. Yet, co-administration of CoQ10 with TiO2NPs and Cd substantially mitigated these adverse consequences. The most notable aspect is that it effectively lowered testicular tissue Ti and Cd levels. It also improved oxidant status, hormonal profile, and sperm picture. CoQ10 minimized the testicular damage implied by histological examination. Furthermore, CoQ10 significantly diminished TiO2NPs and Cd-induced Caspase-3 and TNF-α immunoexpression in testicular tissue. Conclusion: As a result, CoQ10 could be utilized as a safe remedy to protect male reproductive physiology from TiO2NPs and Cd damage.

Naphthaleneoxypropargyl-Containing Piperazine as a Regulator of Effector Immune Cell Populations upon an Aseptic Inflammation.

This study investigated the effects of aseptic inflammation and heavy metal exposure on immune responses, as well as the potential immunomodulatory properties of the newly synthesized 1-[1-(2,5-dimethoxyphenyl)-4-(naphthalene-1-yloxy)but-2-ynyl]-4-methylpiperazine complexed with ß-cyclodextrin (ß-CD). Aseptic inflammation was induced by a subcutaneous injection of turpentine in rats, while heavy metal exposure was achieved through a daily administration of cadmium chloride and lead acetate. The levels of immune cell populations, including cytotoxic T lymphocytes (CTL), monocytes, and granulocytes, were assessed in the spleen. The results showed that aseptic inflammation led to decreased levels of CTL, monocytes, and granulocytes on the 14th day, indicating an inflammatory response accompanied by a migration of effector cells to the inflamed tissues. The exposure to cadmium chloride and lead acetate resulted in systemic immunotoxic effects, with reduced levels of B cells, CD4+ Th cells, monocytes, and granulocytes in the spleen. Notably, piperazine complexed with ß-CD (the complex) exhibited significant stimulatory effects on CD4+, CD8+, and myeloid cell populations during aseptic inflammation, even in the presence of heavy metal exposure. These findings suggest the potential immunomodulatory properties of the complex in the context of aseptic inflammation and heavy metal exposure.

Alleviative effect of melatonin against the nephrotoxicity induced by cadmium exposure through regulating renal oxidative stress, inflammatory reaction, and fibrosis in a mouse model.

Chronic cadmium (Cd) exposure causes severe adverse health effects on the human body, especially the kidney tissue. Studies have demonstrated oxidative stress to be involved in renal pathological variations after exposure to Cd, but few effective treatments are available for the disease yet. Therefore, the present study was carried out to investigate the potential therapeutic intervention and its underlying molecular mechanisms of melatonin (MT), a natural antioxidant with multiple biological activities, against renal injury caused by Cd exposure in mice. C57BL/6 male mice (eight-week-old) were intragastrically administered with CdCl2, MT, or both for 30 days. Biochemical analysis showed that MT intervention significantly improved the SOD, GSH, and CAT activities while markedly decreasing the kidney MDA content of the mice exposed to Cd. Histological examination indicated that Cd exposure resulted in the atrophy of the renal glomerular, the degeneration and dilation of tubules, and the accumulation of fibrocytes. By contrast, MT administration effectively ameliorated the histological outcome of the injured kidney tissue. Moreover, administrating MT significantly inhibited proinflammatory cytokines TNF-α and iNOS expression in Cd-treated mice. Further, MT treatment markedly suppressed the expressions of renal fibrosis-related factors TGF-ß1, α-SMA, and collagen Ⅰ in the injured renal tissue and the accumulation and development of renal fibrosis. In addition, the administration of MT significantly reduced the expression of caspase-3 and cell apoptotic death in the kidney tissue of Cd-exposed mice. In all, the data showed that MT has a compelling therapeutic potential in alleviating the pathological variations of renal injury caused by Cd exposure.

An Innovative Use of Propolis in the Production of Dipping Sauce Powder as a Functional Food to Mitigate Testicular Toxicity Induced by Cadmium Chloride: Technological and Biological Evidence.

Propolis is a common natural ingredient used in food production, food packaging, and pharmaceutical products. Therefore, the aim of our study was to prepare dipping sauce powders as an innovative functional product with a regular and spicy taste from economical raw materials with high nutritional value. The developed products were fortified with propolis powder at 250, 500, and 750 mg/kg. All studied dipping sauces were subjected to a palatability test, a nutritional evaluation, and a microbiological assay performed during 6 months of storage. In addition, an in vivo study was designed to evaluate the efficacy of these products in preventing the testicular toxicity disorders induced by cadmium chloride (CdCl2) in albino rats. Based on the palatability test, the dipping sauces supplemented with propolis at 250 mg/kg and 500 mg/kg were preferred. Moreover, all samples were safe to consume within 6 months. Biological results showed that all investigated propolis-enriched dipping sauce samples caused an improvement in all CdCl2-induced testicular histopathological and biochemical changes, especially the spicy dipping sauce powder fortified with 500 mg/kg of propolis.

Alternations in interleukin-1ß and nuclear factor kappa beta activity (NF-kB) in rat liver due to the co-exposure of Cadmium and Arsenic: Protective role of curcumin.

Cadmium chloride (Cd) and sodium arsenite (As) are two prominent examples of non-biodegradable substances that accumulate in ecosystems, pose a serious risk to human health and are not biodegradable. Although the toxicity caused by individual use of Cd and As is known, the toxicity of combined use (Cd+As) to mammals is poorly understood. The present study aims to investigate the hepatoprotective effect of curcumin (CUR), a naturally occurring bioactive component isolated from the root stem of Curcuma longa Linn., in preventing liver damage caused by a Cd+As mixture. A group of 30 Sprague-Dawley rats were subjected to intraperitoneal administration of Cd+As (0.44 mg/kg+5.55 mg/kg i.p.) and CUR (100 or 200 mg/kg) for a period of 14 days. The experimental results showed that the animals treated with Cd+As exhibited changes in liver biochemical parameters, inflammation and oxidative stress at the end of the experiment. Administration of CUR significantly reduced inflammation, oxidative stress and lipid peroxidation in the Cd+As plus CUR groups compared to the Cd+As group. Furthermore, histological examination of the liver tissue showed that administration of CUR had led to a significant reduction in the liver damage observed in the Cd+As group. The present study provides scientific evidence for the protective effects of CUR against lipid peroxidation, inflammation, oxidative stress and liver damage induced by Cd+As in the liver of rats. The results of our in vivo experiments were confirmed by those of our molecular modelling studies, which showed that CUR can enhance the diminished antioxidant capacity caused by Cd+As.

Vanillin attenuates CdCl2-induced cytotoxicity in isolated human erythrocytes.

Cadmium is a toxic heavy metal with no physiological role in the human body. Cadmium has high mobility due to its widespread industrial use, with no safe and effective therapeutic management. Cadmium toxicity manifests by increasing oxidative stress in target cells. We have explored the potential role of vanillin, a plant phenolic aldehyde and antioxidant, in mitigating cadmium chloride (CdCl2) induced hemotoxicity using isolated human erythrocytes. CdCl2 was added to erythrocytes, in the absence and presence of vanillin. Incubation of erythrocytes with CdCl2 alone inhibited methemoglobin reductase and enhanced methemoglobin level. Heme degradation and release of free iron (Fe2+), along with protein and membrane lipid oxidation, were also increased. A CdCl2-induced enhancement in reactive oxygen and nitrogen species was also seen, lowering the overall antioxidant power of cells. However, pre-incubation of erythrocytes with vanillin resulted in significant decreased generation of reactive species and prevented heme degradation and heme oxidation. Vanillin augmented the erythrocyte antioxidant capacity and reinstated the activities of major antioxidant, plasma membrane-bound and glucose metabolism enzymes. Scanning electron microscopy showed that CdCl2 treatment led to the formation of echinocytes which was prevented by vanillin. In all cases, no harmful effects of vanillin alone were seen. Thus, vanillin alleviates the toxicity of cadmium and can be potentially employed as a chemoprotectant against the damaging effects of this heavy metal.

Listeria monocytogenes from food and food industry environments with reduced susceptibility to benzalkonium chloride, sodium hypochlorite, and peracetic acid.

The growing number of Listeria monocytogenes strains displaying increased tolerance to sanitizers widely applied in the food industry is becoming a problem. The aims of this study were to evaluate the susceptibility of L. monocytogenes isolates from food and food industry environments to sanitizers (benzalkonium chloride, sodium hypochlorite, peracetic acid, and chlorhexidine) and heavy metals (cadmium chloride), as well as to investigate the presence of the main genes related to efflux pumps. All 82 isolates showed reduced susceptibility to benzalkonium chloride (MIC from 16 to 128 µg mL-1), sodium hypochlorite (MIC of ≥ 2048 µg mL-1), and peracetic acid (MIC from 512 to ≥ 2048 µg mL-1), while 22 isolates showed reduced susceptibility to cadmium chloride (MIC > 70 µg mL-1). Susceptibility to chlorhexidine was found (MIC from 2 to 16 µg mL-1). PCR-based analysis revealed that mdrl and lde genes were harbored by 14.6% (12/82) and 40.2% (33/82) of the isolates, respectively. This study demonstrates the presence of L. monocytogenes from food and food industry environments with reduced susceptibility to sanitizers commonly used in food processing environments, highlighting the importance of continuous monitoring of the tolerance profile of this microorganism to sanitizers, as well as the need for strict control of sanitation conditions in food industries.

Evaluation of an ex vivo fibrogenesis model using human lung slices prepared from small tissues.

BACKGROUND: In recent years, there have been breakthroughs in the preclinical research of respiratory diseases, such as organoids and organ tissue chip models, but they still cannot provide insight into human respiratory diseases well. Human lung slices model provides a promising in vitro model for the study of respiratory diseases because of its preservation of lung structure and major cell types. METHODS: Human lung slices were manually prepared from small pieces of lung tissues obtained from lung cancer patients subjected to lung surgery. To evaluate the suitability of this model for lung fibrosis research, lung slices were treated with CdCl2 (30 µM), TGF-ß1 (1 ng/ml) or CdCl2 plus TGF-ß1 for 3 days followed by toxicity assessment, gene expression analysis and histopathological observations. RESULTS: CdCl2 treatment resulted in a concentration-dependent toxicity profile evidenced by MTT assay as well as histopathological observations. In comparison with the untreated group, CdCl2 and TGF-ß1 significantly induces MMP2 and MMP9 gene expression but not MMP1. Interestingly, CdCl2 plus TGF-ß1 significantly induces the expression of MMP1 but not MMP2, MMP7 or MMP9. Microscopic observations reveal the pathogenesis of interstitial lung fibrosis in the lung slices of all groups; however, CdCl2 plus TGF-ß1 treatment leads to a greater alveolar septa thickness and the formation of fibroblast foci-like pathological features. The lung slice model is in short of blood supply and the inflammatory/immune-responses are considered minimal. CONCLUSIONS: The results are in favor of the hypothesis that idiopathic pulmonary fibrosis (IPF) is mediated by tissue damage and abnormal repair. Induction of MMP1 gene expression and fibroblast foci-like pathogenesis suggest that this model might represent an early stage of IPF.

High-Efficiency and Stable Long-Persistent Luminescence from Undoped Cesium Cadmium Chlorine Crystals Induced by Intrinsic Point Defects.

Application of long-persistent luminescence (LPL) materials in many technological fields is in the spotlight. However, the exploration of undoped persistent luminescent materials with high emission efficiency, robust stability, and long persistent duration remains challenging. Here, inorganic cesium cadmium chlorine (CsCdCl3 ) is developed, featuring remarkable LPL characteristics at room temperature, which is synthesized by a facile hydrothermal method. Excited by ultraviolet light, the CsCdCl3 crystals exhibit an intense yellow emission with a large photoluminescence quantum yield of ≈90%. Different from the reported systems with lanthanides or transition metals doping, the CsCdCl3 crystals without dopants perform yellow LPL with a long duration of 6000 s. Joint experiment-theory characterizations reveal the intrinsic point defects of CsCdCl3 act as the trap centers of excited electrons and the carrier de-trapping process from such trap sites to localized emission centers contributes to the LPL. Encouraged by the attractive fluorescence and persistent luminescence as well as good stability of CsCdCl3 against environment oxygen/moisture (75%), heat (100 °C for 10 h), and ultraviolet light irradiation, an effective dual-mode information storage-reading application is demonstrated. The results open up a new frontier for exploring LPL materials without dopants and provide an opportunity for advanced information storage compatible for practical applications.

Pristane cadmium chloride nanoemulsion accelerates the onset of systemic lupus erythematosus in a C57BL/6 mouse model.

OBJECTIVE: To accelerate the onset of systemic lupus erythematosus in C57BL/6 mice by injecting cadmium chloride nanoemulsion and shorten the traditional modeling time. METHODS: Pristane cadmium chloride nanoemulsion was prepared, and 66 C57BL/6 mice were randomly divided into four groups. The pristane group was intraperitoneally injected with 0.6 mL of pristane blank nanoemulsion, the model group was injected with 0.6 mL of pristane cadmium chloride nanoemulsion, the Cadmium chloride control group was injected with 0.6 mL of cadmium chloride nanoemulsion, and the control group was injected with the same amount of 0.9% sodium chloride solution. Urine protein content, anti-dsDNA antibody content, Th1 cell/Th2 cell ratio, and kidney staining were detected in each group. RESULTS: The model group began to develop disease in the 4th week, the anti-dsDNA antibody level reached 566.71 ± 1.44 ng/L, and the proteinuria reached 245.38 ± 30.54 ng/mL. The model group showed an onset at least 5 weeks earlier than that in the pristane group. There was no significant difference in anti-dsDNA antibody content between Cadmium chloride control group and blank group. At the 12th week, the Th1/Th2 cell ratio in the model group significantly decreased, and the pathological changes in the kidneys were consistent with the typical manifestations of lupus in mouse models. CONCLUSION: These results suggest that cadmium chloride promotes earlier onset of pristane-induced systemic lupus erythematosus in a C57BL/6 mouse model.

Heavy metals biosensor based on defective one-dimensional phononic crystals.

In recent years, the detection of water pollution with low levels of heavy metals has attracted the great attention of many researchers as a result of the imminent danger of this type of pollution to all mankind. Meanwhile, we introduce a theoretical approach based on the one-dimensional phononic crystals (1D-PnCs) with a central defect layer as a novel platform for the highly sensitive detection of heavy metal pollution in freshwater. Therefore, the creation of a resonant peak in the transmittance spectrum related to this defect layer is highly conceivable. In this regard, the detection of cadmium chloride (CdCl2) as a dangerous, toxic, and extremely hazardous heavy metal could be investigated based on the small displacement in the position of this resonant peak with the changes in the CdCl2 concentration. Notably, any change in CdCl2 concentration has a direct impact on its acoustic properties. The theoretical framework of our research study is essentially based on the 2 × 2 transfer matrix method and the acoustic properties of the constituent materials as well. The optimization of all sensor parameters represents the mainstay of this study to get the best sensor performance. In this regard, the proposed sensor has a remarkably high sensitivity (S = 1904.25 Hz/ppm) over a concentration range of 0 - 10000 ppm. In addition, the sensor has a high quality factor (QF), and figure of merit of 1771.318, and 73529410-5 (ppm-1), respectively. Finally, we believe this sensor could be a key component of a feasible platform for detecting low concentrations of different heavy metal ions in freshwater.

Impact of bone marrow mesenchymal stem cells on the submandibular gland structure of adult male albino rats exposed to cadmium chloride toxicity.

OBJECTIVE: This study was carried out in submandibular salivary glands of rats to demonstrate the changes induced by cadmium intoxication and the possible prophylactic and therapeutic effects of bone marrow mesenchymal stem cells (BMSCs). DESIGN: Sixty-five rats were divided into five groups. Rats in Group I were controls while those of Group II received daily dose of 10 mg/kg cadmium for 24 days. Rats in Group III received single prophylactic dose of 1 × 106 BMSCs one week before cadmium administration. Rats of Group IV were concomitantly administered cadmium and BMSCs, while those of Group V received cadmium for 24 days and were then treated with single dose of 1 × 106 BMSCs. Rats of Groups I, II, III, and IV were euthanized at the end of the experiment while those of Group V were euthanized one week later. Salivary gland specimens were processed and stained with H&E and inducible nitric oxide synthase; other specimens were used to demonstrate metallothionein gene expression using RT-PCR, malondialdehyde and catalase enzymes were detected by ELISA. RESULTS: Groups III and IV had nearly comparable findings to Group I regarding histological pattern with normal gland features. Group III recorded a lower fold of change for metallothionein gene (1.14 ± 0.20), a lower malondialdehyde enzyme (21.67 ± 1.63 nmol/mg), and a higher catalase enzyme (66.33 ± 2.16 mmol/mg). Regarding all variables, significant differences were found between the different groups (P < 0.001). CONCLUSION: BMSCs have prophylactic and therapeutic effects against cadmium-induced cytotoxicity in rat salivary glands.

Evaluation of Hepatoprotective Efficacy of a Polyherbal Unani Formulation Majoon-Najah against Cadmium Chloride-induced Liver Damage.

BACKGROUND: Majoon-Najah is a composite Unani formulation that consists of multiple medicinal plants and is advised for neurological illnesses. Several studies were carried out on Majoon-Najah (MN) and its ingredients to evaluate the protective effect against seizure and antidepressant activity in animals using a classical form as well as extract. Terminalia bellerica and Emblica officinalis are the major constituents of MN. Scientifically documented literature summarises the hepatoprotective potential of these constituents. AIM: The current study aimed to evaluate the possible hepatoprotective, antioxidant and antiinflammatory perspective of traditional Indian Unani formulation MN and Majoon-Najah hydroalcoholic extract (MNHE) in a Guinea pig model. METHODS: Thirty adult male albino guinea pigs were randomly assigned into five groups for this study. MN and MNHE were given intragastrically for 15 days, followed by intraperitoneal Cadmium chloride (CdCl2, 3 mg/kg/day) from days 8 to 15, as per the schedule. Blood samples were taken from the heart on the 16th day, and the liver was operated on for biochemical analysis and histopathology under complete anesthesia. RESULTS: CdCl2 changed the levels of liver function markers, serum biochemical indicators like albumin, total protein, glucose, and cholesterol in the blood; lipid peroxidation (MDA), glutathione reductase (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPX) in hepatic tissue homogenate, pro-inflammatory cytokines level and liver cytoarchitecture. MN and MNHE were found to protect guinea pigs' liver from CdCl2-induced injury by lowering raised parameters and increasing enzymatic antioxidants. MN and MNHE did not significantly heal injured liver tissues caused by CdCl2 in histopathological examinations. CONCLUSION: CdCl2 induces hepatotoxicity that is likely to worsen with increasing dosage and duration of exposure. MN and MNHE exert their hepatoprotective action by scavenging free radicals, decreasing malondialdehyde levels, activating antioxidant enzymes, and down-regulating proinflammatory indicators.

A Mixture of Multi-Strain Probiotics (Lactobacillus Rhamnosus, Lactobacillus Helveticus, and Lactobacillus Casei) had Anti-Inflammatory, Anti-Apoptotic, and Anti-Oxidative Effects in Oxidative Injuries Induced By Cadmium in Small Intestine and Lung.

INTRODUCTION: Cadmium (Cd) produces severe oxidative stress, which can result in serious clinical consequences and tissue injury. The aim of the present survey was to investigate the protective effects of native Iranian probiotics (Lactobacillus rhamnosus, L. helveticus, and L. casei) against cadmium (Cd)-induced toxicity against the small intestine and lung at histopathological and biochemical levels. MATERIALS AND METHODS: Twenty-one adult male Wistar rats were randomized into three groups of seven rats (control, Cd-treated (3 mg/kg), and concomitant Cd and mix probiotic treatment for 30 days). Histological alterations were appraised via hematoxylin & eosin, Trichrome Masson, and PAS staining. The qRT-PCR technique was applied to assess the expression of pro-apoptotic, anti-apoptotic, and pro-inflammatory genes. Antioxidant enzymes activity was measured via ZellBio kits. RESULTS: Probiotic-treated rats displayed low production of lipid peroxides, reduced malondialdehyde (MDA) level, and elevated contents of superoxide dismutase (SOD) and catalase (CAT) enzymes compared with Cd-treated rats. The results of qRT-PCR demonstrated the up-regulation of Bax, p53, and caspase 3 and down-regulation of Bcl2, TNF-α, and IL-6 genes in both the intestine and lungs of mix probiotic-treated rats compared with Cd-treated animals. Histopathological findings revealed that the probiotic formulation improved Cd-triggered tissue damage in the intestine and lungs. CONCLUSION: The strong cytoprotective benefits of Iranian probiotics against Cd-induced tissue injury observed in this study may be due to their anti-inflammatory and antioxidant properties. Therefore, additional clinical and experimental research is required to explain the precise mechanisms of probiotics' beneficial impacts and underline their potential therapeutic use.

Antioxidant capacity of N-acetylcysteine against the molecular and cytotoxic implications of cadmium chloride leading to hepatotoxicity and vital progression.

Many studies have reported that cadmium (Cd) can induce liver cell injury; however, the toxicity mechanisms of Cd on the liver have not been fully explained. Thirty-two male albino rats were divided into four groups: the control group, the N-acetylcysteine (NAC) group orally as effervescent instant sachets with a concentration of 200 mg dissolved in distilled water and dosage was 200 mg/kg body weight freshly prepared, the cadmium chloride (CdCl2) group (treated with 3 mg/kg orally), and the N-acetylcysteine (NAC) + cadmium chloride group (treated with 200 mg/kg orally post to CdCl2) for 60 days. The NAC alone did not make notable changes in most of the parameters. The CdCl2 alone, compared to control, induced significant alterations in oxidative stress markers (increment in lipid peroxidation (LPO) and nitric oxide (NO)) and antioxidant defense system (decrement in superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx)), which resulted in a downregulation of pro-apoptotic Bcl2-associated X protein (Bax) and caspase-3 and upregulation of anti-apoptotic B-cell leukemia/lymphoma 2 (Bcl2) protein as well as the survival fate of hepatic cells. Post-administration of NAC to CdCl2 resulted in a reduction in oxidative stress markers, shifting of cells from the G2/M phase to the G0/G1 inhibiting signal-regulated kinase activation, and impairment of the anti-apoptotic signaling pathway when compared to the CdCl2 group alone. Accordingly, the Bcl2/Bax ratio was reduced to 1.17-fold change, as an adaptive process to hepatic tissue injury. These findings demonstrated that NAC would attenuate the possibility of oxidative stress and cytotoxicity of hepatic tissue induced by CdCl2.

An assessment of the ameliorative role of hesperidin in Drosophila melanogaster model of cadmium chloride-induced toxicity.

Cadmium chloride (CdCl2) is an important heavy metal widely regarded as an environmental contaminant. Hesperidin, a flavanone glycoside found in citrus fruits, has an established properties against free radicals, apoptosis, and inflammation. The present study investigated the protective actions of hesperidin on CdCl2-induced oxidative damage and inflammation in Drosophila melanogaster. For 7 consecutive days via their diet regimen, the flies were exposed to CdCl2 alone (0.05 mM) or in combination with hesperidin (50 and 100 µM). Exposure to CdCl2 significantly (p < 0.05) increased mortality rate of flies, whereas the survived flies demonstrated significant oxidative toxicity from decreased activities of catalase and Glutathione S-transferase (GST) and Total Thiol (T-SH) and Non-Protein Thiols (NPSH) levels as well as accumulation of Nitric Oxide (NO (nitrite/nitrate)), protein carbonyl and Hydrogen Peroxide (H2O2). However, hesperidin-supplemented diet improved Acetylcholinesterase (AChE) activity, mitochondrial metabolic rate (cell viability), locomotor activity, and amelioration of oxidative damage and lipid peroxidation induced by CdCl2. The hesperidin diet supplement boosted the antioxidant milieu and ameliorated the oxidative damage in the treated flies. Overall, the findings revealed that hesperidin improved antioxidative protective capacity in Drosophila melanogaster model of CdCl2-induced toxicity. This suggests hesperidin as a potential therapeutic agent against oxidative stress disorders due to exposure to CdCl2 and or related toxicants.