Toxicity In Male Rats Research Articles

Effects of environmental bisphenol S exposure on male rat reproductive health and gut-blood-testicular axis integrity.

In this study, male Sprague-Dawley (SD) rats were exposed to bisphenol S (BPS) at environmentally relevant concentrations to investigate its reproductive toxicity and evaluate its effects on the gut-blood-testicular axis. After 28 days of exposure to BPS (0.05 and 20 mg/kg), the results showed a reduction in weight gain and the induction of reproductive toxicity in male rats, including decreased sperm parameters, lower sperm viability, and increased abnormal sperm density and mortality. These observations were made by counting with a hemocytometer under the optical microscope. 16S rRNA and untargeted metabolomic elucidated potential impacts on the gut-blood-testicular axis: BPS impaired the physical barrier, evoked inflammation, and resulted in dysbiosis of the gut microbiota. Additionally, BPS altered serum metabolites, including phosphatidic acid and diacylglycerol, which are involved in Fc gamma R-mediated phagocytosis and linked to inflammation. Furthermore, histopathological analysis, western blot (WB), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence results showed that exposure to BPS led to testicular damage, inflammation, activation of the p38 and ERK MAPK pathways, and disruption of the blood-testis barrier (BTB). Collectively, these findings indicate that BPS impair the intestinal health, disrupt gut microbiome, and ultimately lead to reproductive dysfunction through the gut-blood-testicular axis.

Clinicopathological Studies on the Impact of Grape Seed Extract and L-Carnitine as Cardioprotective Agents Against Doxorubicin-Induced Toxicity in Rats.

Doxorubicin (DOX) cancer therapy induces serious cardiotoxicity as a side effect. This study aimed to investigate the cardioprotective effects of grape seed extract (GSE) and L-Carnitine (L-CA) against DOX-induced cardiac toxicity in male rats. Six groups of male albino rats were used: G1 (control); G2 (GSE), given grape seed extract (100 mg/kg b.wt.) orally for 35 days; G3 (L-CA) (150 mg/kg b.wt.); Group 4 (DOX-induced cardiotoxicity), given DOX (10 mg/kg b.wt., i.p.) on the 28th day of the experiment; G5 (GSE + DOX), given GSE and DOX as previously mentioned; and G6 (L-CA + DOX), given L-CA and DOX as previously mentioned. Electrocardiographic evaluation, lipid profile, lipid peroxidation and antioxidants, serum cardiac markers, and inflammatory markers were estimated. Histopathological evaluation of cardiac tissue was also examined. Key findings showed that DOX induced ECG abnormalities lipid peroxidation, reduced antioxidants, and elevated cardiac and inflammatory markers. GSE and L-CA significantly ameliorated ECG abnormalities, reduced lipid peroxidation, improved antioxidant enzymes and serum cardiac markers, and reduced inflammation. These findings suggest that GSE and L-CA exhibit substantial cardioprotective effects in DOX-induced cardiotoxicity via their antioxidant and anti-inflammatory potentials.

Effects of Flurochloridone on the Developmental Toxicity in Zebrafish (Danio rerio) Embryo.

Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4-144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC50) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1-Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.

The Preventive Effect of Zinc Sulfate against Olanzapine-Induced Testicular Toxicity in Male Rats.

Male infertility is a complex and multifactorial clinical condition affecting a large population attributed to several factors, including perturbation in oxidative stress and the level of essential trace elements. Oxidative stress exerts multiple issues related to reproductive health, including male infertility, decreased sperm motility, sperm DNA damage, and an increased susceptibility to genetic disorders. Besides chemical toxins and food allergens in junk food items, many drugs can also lead to male infertility. Olanzapine (OLZ), a general antipsychotic drug, has also been reported to induce male fertility. A great deal of literature entails that supplementation of zinc can alleviate oxidative stress-related clinical complications, including male infertility. This study investigates the potential protective effects of zinc sulfate (ZnSO4) on OLZ-induced male infertility. In the present study, there were four treatment groups (n = 6): group 1 as control (without any treatment); group 2 treated with OLZ (10mg/kg) orally daily for 6weeks; groups 3 and 4 treated with 50mg/kg and 100mg/kg of ZnSO4 respectively in pre-exposed OLZ (10mg/kg) orally daily for 6weeks. After completion of the treatment, the biochemical analysis of serum and tissue samples demonstrated that group 2 had compromised levels of antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)) as well as elevated levels of stress parameters (oxidized glutathione (GSSG), malondialdehyde (MDA), and nitric oxide (NO)) as compared to the control by a significant extent (p ≤ 0.05). However, supplementation of ZnSO4 significantly corrected all these parameters in a dose-dependent way in groups 3 and 4 (p ≤ 0.05). Other health indicators, like taurine, enzyme Q10, phosphatidylcholine, ascorbic acid, and vitamin E, were also observed to improve prominently with the supplementation of ZnSO4. Intriguingly, all the fertility parameters (sperm motility, count and level of testosterone) were also found to be significantly enhanced with decreased sperm abnormalities in both the combination groups. The histological evaluation of the testis section also agreed with the biochemical analysis in this investigation. Therefore, the study strongly advocates that supplementation of Zn can ameliorate OLZ-induced male infertility to a significant extent.

Hyperpolarization‐activated cyclic nucleotide‐gated channel inhibitor, Ivabradine, attenuates brain mitochondrial oxidative stress without reducing cognitive impairment in Dox‐induced chemobrain

AbstractBackgroundDoxorubicin (Dox), a chemotherapeutic agent, is known to cause chemobrain leading to cognitive decline and brain mitochondrial dysfunction. Ivabradine (Iva), hyperpolarization‐activated cyclic nucleotide‐gated channel blocker used for angina and arrhythmia, has been shown to be an anticonvulsant, antioxidant, and neuroprotective agent. However, the effects of Iva on cognitive function, and brain mitochondrial function in Dox‐induced chemobrain are still not determined. This study aimed to investigate whether Iva attenuates Dox‐induced brain toxicity in male rats by affecting cognitive dysfunction, synaptic dysplasticity, and brain mitochondrial dysfunction.MethodTwenty male Wistar rats were divided into 4 groups: vehicle‐treated control, Iva‐treated control, vehicle‐treated Dox, and Iva‐treated Dox. The control rats were received normal saline, while the Dox‐treated rats were received Dox at a dose of 3 mg/kg/day intraperitoneally on days 0, 4, 8, 15, 22, and 29. Iva (10 mg/kg) was administered by oral gavage from day 0 to day 29. On day 30, novel object location (NOL) test was performed to assess cognitive function. Hippocampal‐synaptic plasticity and brain mitochondrial function were measured after euthanasia.ResultDox‐treated rats showed a decreased % preference index of a new location in the NOL test, decreased % of field excitatory postsynaptic potential (fEPSP), and impaired brain mitochondrial function as indicated by increased mitochondrial ROS, impaired brain mitochondrial membrane potential change, and caused mitochondrial swelling (Figure 1A‐G). Iva‐treated control rats showed no effects on the NOL, % fEPSP, and brain mitochondrial function compared to vehicle‐treated control rats. Iva‐treated Dox rats exhibited a decrease in brain mitochondrial reactive oxygen species (ROS), but showed no significant difference in NOL, % fEPSP, brain mitochondrial membrane potential change, and mitochondrial swelling compared to vehicle‐treated Dox rats (Figure 1A‐G).ConclusionDox‐induced chemobrain manifested in cognitive impairment, synaptic dysplasticity, and brain mitochondrial dysfunction. Iva treatment showed a reduction in brain mitochondrial ROS, with no improvement in mitochondrial membrane potential changes and swelling in Dox‐induced chemobrain. Iva did not improve cognitive function and hippocampal‐synaptic plasticity in Dox‐treated rats. These findings suggest the antioxidant properties of Ivabradine in chemobrain, but this dose of Iva was not enough to protect brain injury in Dox‐induced chemobrain.

Diallyl disulfide prevents cadmium-induced testicular injury by attenuating oxidative stress, apoptosis, and TLR-4/NF-κB and JAK1/STAT3 signaling and upregulating SIRT1 in rats

BackgroundCadmium (Cd) is a heavy metal environmental pollutant that can cause serious health problems. Cd can cause structural changes in the testes and exposure to this heavy metal is associated with the loss of sperms and male infertility. The role of oxidative stress and inflammation in Cd toxicity has been acknowledged. Diallyl disulfide (DADS), an organo-sulfur compound found in garlic, possesses antioxidant, anti-inflammatory, and cytoprotective effects. This study evaluated the protective effect of DADS against Cd reproductive toxicity in male rats, emphasizing the involvement of redox imbalance, TLR-4/NF-κB and JAK1/STAT3 signaling, and SIRT1. MethodsDADS (10 mg/kg body weight) was administered orally to rats for 14 days and a single dose of Cd (1.2 mg/kg) was injected intraperitoneally on day 7. Blood and samples from the testes were collected for analysis. ResultsCd caused testicular injury manifested by multiple histopathological changes and loss of sperms from seminiferous tubules. Circulating levels of gonadotropins and testosterone were decreased in Cd-administered rats. DADS prevented Cd-induced testicular injury and ameliorated serum levels of gonadotropins and testosterone. Cd increased testicular reactive oxygen species (ROS) and malondialdehyde (MDA) and upregulated TLR-4, NF-κB, pro-inflammatory cytokines, JAK1 and STAT3 phosphorylation, Bax and caspase-3, while decreased antioxidants and Bcl-2. DADS effectively decreased ROS and MDA, downregulated TLR-4, NF-κB, JAK1, STAT3, pro-inflammatory cytokines and pro-apoptosis markers in Cd-administered rats. In addition, DADS enhanced antioxidants, Bcl-2, SIRT1 and cytoglobin in the testis of Cd-administered rats. ConclusionDADS prevents Cd-induced testicular injury by attenuating oxidative stress, apoptosis, and TLR-4/NF-κB and JAK1/STAT3 signaling, and upregulating SIRT1 and antioxidants.

Lecithin’s antioxidant properties protect against cyclophosphamide-induced reproductive toxicity and infertility in male rats

Background: Infertility is a prevalent problem that affects 15% of couples globally. Male infertility, which accounts for half of all cases, can be caused by several factors, including aging, drug use, genetic problems, and exposure to environmental toxins. Cyclophosphamide (CP) is a commonly utilized immunosuppressant and anticancer medication that can induce oxidative stress and harm the reproductive system of men. The beneficial effects of antioxidants in mitigating the CP-induced reproductive toxicities are well-documented. Aim: The aim of this study was to assess the effects of lecithin (as an antioxidant) against the CP-induced reproductive toxicity in male rats. Methodology: Thirty Sprague-Dawley male rats were divided into three groups: (i) the negative control group (that received sterile water via the intragastric route for 13 consecutive days), (ii) the positive control group (that received sterile water via the intragastric route for 5 days and, subsequently, a single, intraperitoneal dose of CP on day 6, followed by sterile water via the intragastric route for the next 7 consecutive days), and (iii) the lecithin-treated group (that received lecithin via the intragastric route for 5 days and, subsequently, a single, intraperitoneal dose of CP on day 6, followed by lecithin via the intragastric route for the next 7 consecutive days). Results: Lecithin treatment improved sperm parameters, plasmatic testosterone levels, and glutathione peroxidase, thereby preventing histopathological alterations in the rat testes. Conclusion: Lecithin demonstrated its potential protective effects against reproductive impairments and oxidative stress in the CP-treated rat group, and might prove promising for use in clinical practice as a protective agent against chemotherapy-induced male reproductive toxicity and infertility.

Reproductive and developmental toxicity of α-terpineol in Wistar rats

Alpha-terpineol (α-T) is a type of monoterpenoid alcohol commonly present in essential oils, it contributes to a pleasant floral fragrance similar to that of lilacs. This research aimed to evaluate the impact of α-terpineol on the reproductive functions of both male and female rats, including gonadal activity, mating behavior, conception, conceptus development and parturition. Six male and female Wistar rats per group received α-terpineol through gavage at doses of 0, 75, 150 and 300 mg/kg/day. The study revealed changes in body weight gain inhibition, food consumption, azoospermia, decreased testosterone levels (0.7 ± 1.61 ng/mL, 0.7 ± 2.30 ng/mL) as well as histopathological variations in testis and epididymis among males exposed to doses of 150 and 300 mg/kg/day. Moreover, this exposure led to significantly decreased serum T4 levels in both adult males (21.85 ± 12.68 ng/mL, 16.20 ± 9.15 ng/mL) and dams (11.24 ± 12.37 ng/mL, 9.48 ± 11.74 ng/mL) at the dose range of 150 and 300 mg/kg/day without affecting TSH concentrations. In summary, the present study showed that α-terpineol induced reproductive toxicities in male rats. Therefore, a detailed toxicological assessment is highly recommended.

Metabolome classification of Tongkat Ali (Eurycoma longifolia jack) and its commercial products via UHPLC-QTOF-MS-MS and its protective effect against 5-flurouracil-Induced testicular toxicity in male rats

Ethnopharmacological relevanceTongkat Ali (Eurycoma longifolia Jack) is a chief herbal medicine that is well recognized for its aphrodisiac properties, available in various commercial products worldwide. Aim of the studyThe aim of this work is to identify the different classes of secondary metabolites present in Tongkat Ali commercial products versus authenticated root, and to assess its root extract mitigative effect against 5-flurouracil (5FU)-induced testicular toxicity. Materials and methodsHigh-resolution UHPLC-QTOF-MS/MS metabolites analysis was utilized on the ethanolic Tongkat Ali extract (TAE) parallel to three Mlayasian commercial products, followed by a multivariate data analysis to understand the variability among UHPLC-MS metabolites datasets. Adult male rats were treated with 5-Fluorouracil (5FU) ± Tongkat Ali extract. Semen parameters, serum testosterone, LH, and FSH, and testicular oxidative stress biomarkers like malondialdehyde (MDA) levels, Nuclear factor kappa B (NF-κB) and erythroid 2–related factor 2 (Nrf2) were analyzed. ResultsThe main categories of secondary metabolites identified through UHPLC-MS/MS profiling were quassinoids, alkaloids, fatty acids, lignans and coumarins. Long Jack Plus® ELP-2 clustered alongside authentic roots ELR on the negative side, while Naturelle® ELP-1 and Nu-Prep-LEAKI® ELP-3 were positioned on the opposite side. The OPLS-DA model was used to identify markers for preparations from authentic roots, with commercial products enriching in ailanthone epoxide. In vivo results showed that 5FU reduced sperm parameters by 42%, while TAE improved sperm quality by 35–43% and 58–74% at dose of 400 and 800 mg/kg, respectively. Testosterone, reduced by 74% with 5FU, increased 2.3- to 3.2-fold with TAE. TAE also reduced MDA by 31–62%, NF-κB by 32–55% and increased Nrf2 by 1–2 folds. ConclusionThe manuscript presents a comparative metabolomics study and in vivo investigation into the potential of Tongkat Ali root to improve testicular function in male rats intoxicated with 5FU, an area not previously explored. Further research is required to understand the mechanisms.

Ameliorative effect of Melatonin on 5-Fluorouracil-induced reproductive toxicity in male rats.

5-Fluorouracil (5-FU) is an antimetabolite chemotherapeutic agent that can cause oxidative stress and complications in normal organs, including the reproductive system. This study was conducted to investigate the effect of melatonin (MEL) on 5-FU-induced reproductive toxicity in male rats. Male Wistar rats weighing 180 ± 20g were divided into five groups: control, 5-FU (50mg/kg), 5-FU + MEL (2.5, 5 & 10mg/kg). The testes and prostates were removed, and histopathological aspects, biochemical markers, and gene expression were investigated. The effect of 5-FU on the normal TM4 cell line (murine testicular Sertoli line) and co-treatment of 5-FU and MEL were studied using MTT assay. Results showed that MEL prevented cell death in the TM4 cell line induced by 5-FU. MEL also reduced edema, hyperemia, and vacuolization in testis and prostate tissues induced by 5-FU. Additionally, MEL increased the activity of antioxidant enzymes and reduced the levels of MDA (p < 0.0001) and MPO (p < 0.0001). The levels of testosterone (p < 0.01) and the number of spermatocytes and spermatogonia (p < 0.0001) were increased in groups receiving 5-FU with MEL compared to 5-FU alone. The prostate-specific antigen (PSA) level in prostate samples was lower in the groups receiving 5-FU with MEL compared to the 5-FU group. Furthermore, the genes expression of COX-2 and TNF-α in testis tissues was reduced in the presence of MEL. in conclusion, the antioxidant property of MEL can protect the male reproductive system against 5-FU toxicity, as evidenced by the improved histopathological and biochemical parameters, as well as the reduced gene expression of COX-2 and TNF- α genes.

Ameliorative Effect of Vitamin C against Hydroxyurea-Induced Hepatic Toxicity in Male Rats

Ameliorative Effect of Vitamin C against Hydroxyurea-Induced Hepatic Toxicity in Male Rats

Ameliorative action of eugenol on nitrate induced reproductive toxicity in male rats

There is a great concern for studies to prevent nitrate (NO3) induced male reproductive toxicity as it might lead to infertility. Therefore, the study was aimed to investigate the ameliorative effects of eugenol on NO3 induced male reproductive toxicity in wistar rats. Adult male rats were randomly divided into five groups (n=5). The first group was served as control, the second and third group of rats were treated with 100 mg/kg bw of sodium nitrate (NaNO3) and NO3 contaminated ground water respectively. The fourth and fifth group of rats were orally intubated with eugenol (100 mg/kg bw) and then exposed to NaNO3 and NO3 contaminated ground water respectively. The treatment was continued for 52 days. Nitrate exposure significantly decreased the sperm motility, testicular 3-beta-hydroxysteroid dehydrogenase activity, serum concentration of testosterone, activities of superoxide dismutase and catalase in testis and spermatozoa and different categories of germ cells in stage VII of spermatogenesis. Further, there was significant increase in sperm abnormality and levels of nitrite (NO2) and malondialdehyde in testis and spermatozoa of NO3 treated rats. In addition, NO3 exposure distorted the histological architecture of seminiferous tubules of testis. It was established that NO3 induced high production of NO2 affected spermatogenesis, steroidogenesis and sperm motility. However, in the present study, pretreatment of eugenol prevented NO3 induced reproductive alterations by decreasing the level of NO2. These findings clearly showed the protective action of eugenol against NO3 induced oxidative stress in male reproductive system.

Role of Spirulina platensis on some Physiological Aspects in Paracetamol-Induced Subacute Toxicity in Male Rats

Role of Spirulina platensis on some Physiological Aspects in Paracetamol-Induced Subacute Toxicity in Male Rats

Hesperidin neuroprotective effects against carbon monoxide-induced toxicity in male rats.

Carbon monoxide (CO) is produced via incomplete combustion of fossil fuels and it may cause long-term neurological sequel upon exposure. Hesperidin (HES), a flavanone glycoside found in citrus plants, exerts diverse beneficial health effects. The present study mechanistically examined the neuroprotective effects of HES in CO-poisoned rats. Thirty male Wistar rats (five groups of six animals) were exposed to 3000 ppm CO for 1 h. Immediately after the exposure and on the next 4 consecutive days (totally five doses), rats intraperitoneally received either normal saline (the control group) or different doses of HES (25, 50, and 100 mg/kg). A sham group that was not exposed to CO was also considered. After evaluation of spatial learning and memory using a Morris water maze (MWM), animals were sacrificed and oxidative stress status in blood samples, and Akt, Bax, Bcl2, and brain-derived neurotrophic factor (BDNF) expression in brain samples were assessed. Western blot analysis indicated increased Akt but decreased Bax/Bcl2 levels in the HES 100 mg/kg, and induced BDNF levels in all HES-treated groups. MWM results showed that HES significantly decreased memory loss. The current findings indicate that HES could alleviate neurological impairments induced by CO in rats.

Protective effect of Petroselinum crispum methanolic extract against acrylamide-induced reproductive toxicity in male rats through NF-ĸB, kinesin, steroidogenesis pathways

This study examined the protective effects of a Petroselinum crispum (P. crispum) methanolic extract on reproductive dysfunction induced by acrylamide in male rats. A total of 40 rats were divided into four groups (n=10). The control group received distilled water, the acrylamide group received 10 mg/kg of acrylamide, the P. crispum group received 100 mg/kg of P. crispum extract, and the combined group was pretreated with P. crispum for two weeks before co-administration of P. crispum and acrylamide. All administrations were administered orally using a gastric tube for eight weeks. Acrylamide decreased testosterone levels but did not affect levels of FSH or LH. It also increased testicular levels of (MDA) malondialdehyde and reduced activity of (SOD) superoxide dismutase and impairment of sperm parameters. Furthermore, the administration of acrylamide resulted in an elevation of tumor necrosis factor-alpha (TNF-α) levels and a reduction in the levels of steroidogenic acute regulatory protein (STAR) and cytochrome P450scc (P450scc). Acrylamide negatively affected the histopathological outcomes, Johnsen's score, the diameter of seminiferous tubules, and the thickness of the germinal epithelium. It also upregulated the expression of NF-ĸB P65 and downregulated the expression of kinesin motor protein. In contrast, treatment with P. crispum extract restored the levels of antioxidant enzymes, improved sperm parameters, and normalized the gene expression of TNF-α, IL-10, IL-6, iNOS, NF-ĸB, STAR, CYP17A1, 17β-HSD and P450scc. It also recovered testicular histological parameters and immunoexpression of NF-ĸB P65 and kinesin altered by acrylamide. P. crispum showed protective effects against acrylamide-induced reproductive toxicity by suppressing oxidative damage and inflammatory pathways.

Potential protective role of carob ethanolic extract against diclofenac sodium-induced acute hepatorenal toxicity in male rats: Biochemical and Histopathological studies

Potential protective role of carob ethanolic extract against diclofenac sodium-induced acute hepatorenal toxicity in male rats: Biochemical and Histopathological studies

Molecular insights into the antioxidative and anti-inflammatory effects of P-coumaric acid against bisphenol A-induced testicular injury: In vivo and in silico studies

This study investigated the protective effects of p-coumaric acid (PCA) against bisphenol A (BPA)-induced testicular toxicity in male rats. The rats were divided into control, BPA, BPA+PCA50, BPA+PCA100, and PCA100 groups. Following a 14-day treatment period, various analyses were conducted on epididymal sperm quality and testicular tissues. PCA exhibited dose-dependent cytoprotective, antioxidant, and anti-inflammatory effects, ameliorating the decline in sperm quality induced by BPA. The treatment elevated antioxidant enzyme activities (SOD, GPx, CAT) and restored redox homeostasis by increasing cellular glutathione (GSH) and reducing malondialdehyde (MDA) levels. PCA also mitigated BPA-induced proinflammatory responses while reinstating anti-inflammatory IL-10 levels. Apoptotic parameters (p53 and p38-MAPK) were normalized by PCA in BPA-treated testicular tissue. Immunohistochemical and immunofluorescent analyses confirmed the cytoprotective and anti-inflammatory effects of PCA, evidenced by the upregulation of HO-1, Bcl-2, and Nrf-2 and the downregulation of the proapoptotic gene Bax in BPA-induced testicular intoxication. PCA corrected the disturbance in male reproductive hormone levels and reinstated testosterone biosynthetic capacity after BPA-induced testicular insult. In silico analyses suggested PCA's potential modulation of the oxidative stress KEAP1/NRF2/ARE pathway, affirming BPA's inhibitory impact on P450scc. This study elucidates BPA's molecular disruption of testosterone biosynthesis and highlights PCA's therapeutic potential in mitigating BPA's adverse effects on testicular function, showcasing its cytoprotective, anti-inflammatory, and hormone-regulating properties. The integrated in vivo and in silico approach offers a comprehensive understanding of complex mechanisms, paving the way for future research in reproductive health and toxicology, and underscores the importance of employing BPA-free plastic wares in semen handling.

Ameliorative effects of zinc and vitamin E against phthalates-induced reproductive toxicity in male rats.

Phthalates (PEs) could cause reproductive harm to males. A mixture of three widely used PEs (MPEs) was used to investigate the ameliorative effects of zinc (Zn) and vitamin E (VE) against male reproductive toxicity. Fifty male SD rats were randomly divided into five groups (n = 10). Rats in MPEs group were orally treated with 160 mg/kg/d MPEs, while rats in MPEs combined Zn and/or VE groups were treated with 160 mg/kg/d MPEs plus 25 mg/kg/d Zn and/or 25 mg/kg/d VE. After intervention for 70 days, it's was measured of male reproductive organs' weight, histopathological observation of sperms and testes, serum hormones, PIWI proteins and steroidogenic proteins. Compared with control, anogenital distance, testes weight, epididymides weight, and sex hormones were significantly decreased, while the sperm malformation rate was markedly increased in MPEs group (p < .05); the testicular tissues were injured in MPEs group with disordered and decreased spermatids, and arrested spermatogenesis. PIWIL1, PIWIL2, StAR, CYP11A1 and CYP19A1 were down-regulated in MPEs group (p < .05). However, the alterations of these parameters were restored in MPEs combined Zn and/or VE groups (p < .05). Zn and/or VE improved steroid hormone metabolism, and inhibited MPEs' male reproductive toxicity.

Ameliorative effects and histological assessment of active fractions of ethanolic fruits extract of Raphia hookeri on AlCl3 induced toxicity in rats

Background: Aluminium chloride is a widely distributed element with a well-established toxicity. The study aimed at evaluating ameliorative effects of active fractions and ethanolic fruits extracts of Raphia hookeri on AlCl3-induced toxicity in male rats. The objectives included; determination of liver and kidney function biomarkers, lipid profile, histopathological assessment of the organs. Methods: A total of 110 healthy male rats weighing 180-200 g were grouped into 11 groups of 10 rats each. Group 1: Normal feed and water (normal control). Group 2: AlCl3 only. Group 3: 200 mg/kg b. w of vitamin C. Group 4 and 5: N-hexane fraction at 10 and 20 mg/kg b. w. Group 6 and 7: ethyl acetate fraction at 10 and 20 mg/kg b. w. Group 8 and 9: Aqueous fractions at 10 and 20 mg/kg b. w. Group10 and 11: Ethanol extract at doses of 200 mg/kg b. w and 400 mg/kg b. w. The treatment lasted for 21 days. Results: Results revealed a significant (p˂0.05) decreased in the activities of ALT, AST, ALP, TB, DB and TP. It further revealed a significant (p˂0.05) decrease in urea, creatinine, sodium, potassium and chloride. Also, a significant (p˂0.05) decrease in CHOL, TG, HDL-C, LDL-C was observed. Histopathological assessment of the liver and kidney tissues corroborated the observed changes in enzymes activities. Conclusions: The findings demonstrated ameliorative potentials of active fractions and ethanolic fruit extract of Raphia hookeri against hepatic and renal damage induced by AlCl3 in a dose and time dependent manner.

Nephroprotective Effects of Aqueous Extract of Loranthus micranthus Linn Leaf Against Cadmium-Induced Kidney Toxicity in Male Rats

Cadmium is a heavy metal widely distributed in the environment due to anthropogenic activities, such as industrial processes, mining, and agricultural practices. Exposure to cadmium has been associated with various adverse health effects, particularly on the kidneys. The kidneys are major target organs for cadmium toxicity, as the metal tends to accumulate in renal tissues, leading to nephrotoxicity and impaired renal function.This study aims to evaluate the potential nephroprotective effects of the aqueous extract of Loranthus micranthus Linn leaf against cadmium-induced kidney toxicity in a rat model. Twenty-four male rats were divided into four groups: Group 1 served as the normal control and received no treatment. Group 2 was exposed to cadmium toxicity, receiving 2 mg/kg body weight of cadmium intraperitoneally daily. Group 3 received 150 mg/kg body weight of the extract daily. Group 4 received 2 mg/kg body weight of cadmium intraperitoneally, followed by a daily administration of 150mg/kg body weight of the extract. This experiment was carried out for a period of 28 days. Biochemical alterations in serum creatinine, blood urea nitrogen, total protein, superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and malondialdehyde (MDA) were assessed as markers of kidney function and oxidative stress. Additionally, ultrastructural changes in the kidneys of the experimental animals were evaluated using electron microscopy. The study revealed significant biochemical alterations in markers of kidney function and oxidative stress in rats exposed to cadmium-induced kidney toxicity. Treatment with the extract attenuated these biochemical changes, indicating potential nephroprotective effects. Furthermore, ultrastructural changes observed in the kidneys of cadmium-exposed rats were ameliorated by treatment with the extract. The findings of this study suggest that the extract possesses potential nephroprotective effects against cadmium-induced kidney toxicity. Further research is necessary to elucidate the mechanisms of action and explore the therapeutic potential of these natural compounds in managing kidney-related disorders.