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Manganese, an essential nutrient for male reproductive health, exerts dose-dependent effects, with excessive exposure—particularly to manganese dioxide nanoparticles ( MnO 2 -NPs ) from environmental or industrial sources inducing gonadal damage via oxidative stress, hormonal disruption, and impaired steroidogenesis. This study evaluated rosemary essential oil ( REO ) against MnO 2 -NP -induced reproductive dysfunction in male rats. Seventy-two Sprague–Dawley rats (130 ± 10 g) were divided into six groups ( n  = 12): Group I (deionized water), Group II (saline), Group III ( MnO 2 -NP , 100 mg/kg bw/day), Group IV ( REO , 250 mg/kg/day), Protective Group V ( REO pre-treatment +  MnO 2 -NPs ), and Therapeutic Group VI ( MnO 2 -NPs + REO co-treatment) for 56 days. MnO 2 -NP exposure caused testicular injury, marked by elevated lipid peroxidation (↑malondialdehyde, ↑nitric oxide), suppressed antioxidants (↓total antioxidant capacity, ↓catalase, ↓glutathione), impaired sperm parameters (motility, count, morphology), and altered serum hormone levels (follicle-stimulating hormone, luteinizing hormone, testosterone). These effects correlated with downregulated steroidogenesis genes ( StAR , HSD-3β , CYP11A1 ). Both Protective and Therapeutic REO treatment mitigated MnO 2 -NPs oxidative stress, restored hormonal balance, and normalized gene expression. Histopathology revealed reduced seminiferous tubule degeneration and enhanced spermatogenesis in REO groups. Findings demonstrate REO’s efficacy in alleviating MnO 2 -NPs induced reproductive toxicity via antioxidant and steroidogenic modulation, positioning REO as a promising therapeutic against nanomaterial-induced gonadotoxicity.

Copper oxide nanoparticles (CuO-NPs) are known to trigger systemic toxicity through the disruption of copper homeostasis and the generation of profound oxidative stress. Given their widespread industrial applications, concerns persist regarding environmental and human exposure. This cascade of molecular injury drives multi-organ damage, immune suppression, and genomic instability. To address this concern, the present study systematically evaluates the potential of engineered curcumin nanoparticles (Cur-NPs) against CuO-NPs-induced toxicity in a rodent model as a proof of principle. Sixty adult male Sprague–Dawley rats were randomized into five experimental groups: control, vehicle (corn oil), CuO-NPs (50 mg/kg), Cur-NPs (50 mg/kg), and CuO-NPs + Cur-NPs co-treatment, administered orally for 30 days. Toxicological endpoints included oxidative stress biomarkers, immune functional assays (total leukocyte count, phagocytic index), regulation of apoptotic pathways (Bax/Bcl-2 ratio, caspase-3 activity), DNA integrity via the alkaline comet assay, and detailed histopathological examination of the liver, kidneys, and spleen. Exposure to CuO-NPs alone triggered severe oxidative damage, marked immunosuppression, a pro-apoptotic imbalance, and significant hepatic DNA fragmentation. Histopathology confirmed systemic injury, including hepatic necrosis, renal tubular degeneration, and splenic lymphoid depletion. Co-treatment with Cur-NPs significantly mitigated these effects, restoring antioxidant defences, immune competence, and apoptotic balance, while reducing DNA damage and tissue pathology. Cur-NPs alone maintained profiles comparable to controls, confirming their safety. Collectively, these findings reveal that Cur-NPs confer potent protection primarily by re-establishing redox homeostasis and modulating critical immune and apoptotic pathways, with copper chelation representing a proposed but unconfirmed contributory mechanism. This study provides a strong rationale for a plant-based, nanomaterial-enabled intervention to systemically protect against engineered nanomaterial toxicity in occupational settings, offering a foundation for developing exposure mitigation strategies. Highlights CuO-NPs provoke systemic toxicity: oxidative stress, immunosuppression, and DNA damage. Cur-NPs attenuate CuO-NPs-induced immunotoxicity, restoring leukocyte counts and phagocytic capacity. Cur-NPs protect against genomic instability, significantly reducing DNA damage. Cur-NPs restore apoptotic signalling equilibrium (Bax/Bcl-2 ratio) and ameliorate histopathological damage in the liver, kidneys, and spleen. Initial validation establishes nano-curcumin as a novel phytochemical for systemic protection in contexts relevant to workplace safety.

The present study was carried out to clarify the effect of different doses of melatonin on some reproductive hormones, serum total antioxidant, histopathological examination, lipid peroxidation, and antioxidant parameters in liver, kidney, heart, and testis tissues in induced-hyperthyroidism (HT) male rat model. A total of 75 mature male Wistar rats were equally allocated into five groups; control groups were daily I/P injected with distilled water containing 4 M ammonium hydroxide in methanol and 1% absolute ethanol; on hyperthyroidism model group, rats received daily I/P injection of L-thyroxine (0.2 mg/kg body weight). In melatonin-treated groups, rats were injected with the same dose of L-thyroxine followed by I/P injection of melatonin (1, 5, or 10 mg/kg, respectively) for 21 days. The hyperthyroidism group showed significant increase in serum thyroxine (T4), triiodothyronine (T3), and testosterone levels and a significant decrease in the levels of thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and serum total antioxidants capacity, with a significant decrease in superoxide dismutase (SOD) activity and glutathione reductase (GSH) content with a significant increase in malondialdehyde (MDA) concentration in all examined tissues. While, melatonin co-treatment to HT groups partially counteracted the effect of hyperthyroidism by decreasing serum T4 and T3 levels and increasing serum TSH. In addition, melatonin could decrease serum levels of FSH, LH, and testosterone, as well as it could increase serum total antioxidants capacity, SOD activity, and GSH content and decreased MDA concentration in all examined tissues. Additionally, melatonin could amend the histopathological alterations in the examined tissues of hyperthyroid rats but not the testicular tissue. It is concluded that melatonin has a protective role against the hyperthyroidism-induced oxidative damage but cannot ameliorate the reproductive disorders in male rat model.

A Correction to this paper has been published: https://doi.org/10.1007/s11356-020-11784-y .

Manganese, an essential nutrient for male reproductive health, exerts dose-dependent effects, with excessive exposure-particularly to manganese dioxide nanoparticles (MnO -NPs) from environmental or industrial sources inducing gonadal damage via oxidative stress, hormonal disruption, and impaired steroidogenesis. This study evaluated rosemary essential oil (REO) against MnO -NP-induced reproductive dysfunction in male rats. Seventy-two Sprague-Dawley rats (130 ± 10 g) were divided into six groups (n = 12): Group I (deionized water), Group II (saline), Group III (MnO -NP, 100 mg/kg bw/day), Group IV (REO, 250 mg/kg/day), Protective Group V (REO pre-treatment + MnO -NPs), and Therapeutic Group VI (MnO -NPs + REO co-treatment) for 56 days. MnO -NP exposure caused testicular injury, marked by elevated lipid peroxidation (↑malondialdehyde, ↑nitric oxide), suppressed antioxidants (↓total antioxidant capacity, ↓catalase, ↓glutathione), impaired sperm parameters (motility, count, morphology), and altered serum hormone levels (follicle-stimulating hormone, luteinizing hormone, testosterone). These effects correlated with downregulated steroidogenesis genes (StAR, HSD-3β, CYP11A1). Both Protective and Therapeutic REO treatment mitigated MnO -NPs oxidative stress, restored hormonal balance, and normalized gene expression. Histopathology revealed reduced seminiferous tubule degeneration and enhanced spermatogenesis in REO groups. Findings demonstrate REO's efficacy in alleviating MnO -NPsinduced reproductive toxicity via antioxidant and steroidogenic modulation, positioning REO as a promising therapeutic against nanomaterial-induced gonadotoxicity.

Background and Aim: Monkeypox (Mpox) is a viral disease mainly found in central and western Africa, with symptoms similar to variola virus (smallpox) but distinguished by the early lymph node swelling specific to Mpox. This review summarizes the neuropsychiatric manifestations of Mpox infection and vaccination, along with management approaches. Method: We searched different databases such as PubMed, Scopus, WoS, and Google Scholar about the neuropsychiatric manifestations of Mpox disease and the associated strategies of management. Results and conclusions: Mpox can cause a wide range of neurological symptoms. These range from mild symptoms like headaches, muscle aches, fatigue, and pain to severe symptoms, including seizures, blindness, photophobia, delirium, coma, encephalitis, and transverse myelitis. It is essential to distinguish Mpox from smallpox and other orthopox viruses. Psychiatric issues, such as stigma, disfigurement, isolation, and physical pain, are common in Mpox patients. To address these, healthcare providers should provide accurate information, counseling, and virtual support. Neurological side effects were associated with the previous smallpox vaccine, which offered cross-protection against Mpox. This vaccine has since been replaced by JYNNEOS, which does not pose any neurological risks. Mpox-related neurological symptoms are generally managed with supportive care, including NSAIDs, antibiotics, antiepileptics, and sedatives for seizures. Antivirals like acyclovir are also used. Severe cases may require hospitalization or intubation. So, we recommend early diagnosis, isolation, and prompt treatment, as Mpox spreading to the central nervous system can lead to serious and potentially fatal complications.

AimTo assess knowledge, attitude and practice (KAP) of antimicrobial self-medication among a convenience sample of population in Alexandria, Egypt.MethodologyA descriptive cross-sectional study using a self-administrated semi-constructed questionnaire. A convenience sample of 359 participants was studied using appropriate consent. The questionnaire had four sections: demographics, KAP, professional medical knowledge and attitude of children caregivers toward antimicrobial self-medication. The questionnaire was initially constructed in English and then translated into its final Arabic version. The Arabic version was pilot-tested and face-validated. Descriptive and quantitative analysis were performed using SPSS (V.20.0).ResultsApproximately 64% (231) of the studied population used antibiotics without prescription in the past 12 months. This was significantly correlated with female gender and lack of knowledge. The main reason for self-medication was due to saving time and effort (109, 47%) followed by not preferring doctor visits (89, 39%). More than 60% of cases used amoxicillin-clavulanic acid. The main sources of antibiotics were leftovers from previously prescribed pharmaceuticals and those purchased from community pharmacies. 85 participants were young children caregivers of which 18 (21%) reported administering antibiotics to their children without consulting a physician. Out of 115 who claimed attaining medical background, only 30 (26%) managed to answer section 3 correctly with 23 of them reporting antibiotic self-medication.ConclusionThis study showed an increased tendency towards antibiotic self-medication among Alexandrian adults and children that was not significantly decreased in population with medical background. The reasons discussed within the study should be further addressed to decrease such practice.