ArticleOncology letters2019
Mechanism of cadmium poisoning on testicular injury in mice.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Potentially Toxic Elements and Male Reproductive Toxicity: Mechanisms, Implications, and Protective Strategies: A Narrative Review.Journal of biochemical and molecular toxicology · 2026Review
- Effects of Excessive Manganese Exposure on Testicular Oxidative Stress, Histopathology, and Nrf2 Signaling Pathway in Mice.Biological trace element research · 2026Article
- Revisiting cadmium-induced toxicity in the male reproductive system: an update.Archives of toxicology · 2024Review
- Egg White Hydrolysate Mitigates Cadmium-induced Neurological Disorders and Oxidative Damage.Neurochemical research · 2024Article
- Comparing the effects ofJournal of advanced veterinary and animal research · 2023Article
- Circulating microRNAs as promising testicular translatable safety biomarkers: current state and future perspectives.Archives of toxicology · 2023Review
- Acetovanillone augmented the cardioprotective effect of carvedilol against cadmium-induced heart injury via suppression of oxidative stress and inflammation signaling pathways.Scientific reports · 2023Article
- The adverse role of endocrine disrupting chemicals in the reproductive system.Frontiers in endocrinology · 2023Review
- Article
- Activated Nrf-2 Pathway by Vitamin E to Attenuate Testicular Injuries of Rats with Sub-chronic Cadmium Exposure.Biological trace element research · 2022Article
- Enhanced Uptake of Arsenic Induces Increased Toxicity with Cadmium at Non-Toxic Concentrations onToxics · 2022Article
- An electron microscopic and biochemical study of the potential protective effect of ginger against Cadmium-induced testicular pathology in rats.Frontiers in physiology · 2022Article
- Establishment of an oligoasthenospermia mouse model based onAnimal models and experimental medicine · 2021Article
- Edible bird's nest protects histomorphology of rat's uterus against cadmium (Cd) toxicity through a reduction of Cd deposition and enhanced antioxidant activity.Saudi journal of biological sciences · 2021Article
- Damage to the Testicular Structure of Rats by Acute Oral Exposure of Cadmium.International journal of environmental research and public health · 2021Article
- Exogenous Factors Affecting the Functional Integrity of Male Reproduction.Life (Basel, Switzerland) · 2021Review
- Therapeutic Effects of Ethanolic Extract ofFrontiers in veterinary science · 2021Article
- Effects of Cadmium, Lead, and Mercury on the Structure and Function of Reproductive Organs.Toxics · 2020Review
- Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice.Biomolecules · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadmium is a heavy metal that is toxic to humans and the reproductive system. The present study aimed to investigate the mechanisms of cadmium-induced reproductive toxicity in a male Institute of Cancer Research mouse model of cadmium poisoning. Changes in luteinizing hormone receptor (LHR), 17α-hydroxylase and endothelial nitric oxide (NO) synthase (eNOS) expression levels were examined. A total of 24 male mice (4-week-old) were randomly divided into four groups (normal control group and low, medium and high cadmium groups) and subjected to gavage treatment with normal saline or cadmium-containing saline solutions for 8 weeks prior to sacrifice. To assess testicular injury, serum androgen levels were determined by ELISA, testicular tissue pathological changes were evaluated using hematoxylin and eosin staining. In addition, LHR, 17α-hydroxylase and eNOS expressions levels were examined by western blotting, and apoptosis was examined with a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The results demonstrated that the severity of testes injury increased with cadmium concentration. In addition, LHR, 17α-hydroxylase and eNOS expression levels increased with low and medium concentrations of cadmium; however, they were decreased following treatment with high concentrations of cadmium. The results from the present study demonstrated that cadmium altered LHR, 17α-hydroxylase and eNOS expression levels in testicular stromal cells, which may impact testosterone synthesis. Furthermore, NO was suggested to be involved in cadmium-induced testicular injury by measurements of eNOS expression in testicular stromal cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.