The prevalence of low back pain associated with disc degeneration reduced quality of life with socio-economic impact. This study is aimed at investigating the histomorphometric and antioxidant response of Brassica oleracea extract in annular puncture-induced intervertebral disc degeneration using a rabbit model. Fifteen (15) New Zealand white rabbits were used in this study and were divided into five groups (n = 3). Group A (non-punctured) received distilled water as placebo; group B underwent annular puncture for 4 weeks; group C underwent annular puncture for 8 weeks; group D underwent annular puncture for 2 weeks before receiving 500 mg/kg bw of Brassica oleracea extract for 2 weeks; group E underwent annular puncture for 4 weeks before receiving 500 mg/kg bw of Brassica oleracea extract for 4 weeks. The rabbits were sacrificed at 4 and 8 weeks after treatment, the discs were extracted and the histological, stereological and biochemical analysis were performed. Histological results showed lack of NP cells, disorganization in the arrangement of collagen fibres in the punctured control group (groups B and C), which was restored by Brassica oleracea extract administration after 2 and 4 weeks of treatment in the punctured-treated groups (D and E). Oxidative stress markers (CAT, SOD and GSH) levels were significantly reduced with corresponding increase in MDA among punctured-control groups but restored after 2 and 4 weeks of treatment in the punctured-treated groups. Administration of Brassica oleracea extract revealed a preventive and restorative potential in the cytoarchitecture and antioxidant level of the disc induced by annular puncture.

Background Cisplatin‑evoked neurotoxicity largely arises from excessive oxidative‑nitrosative stress, causing cerebellar neurodegeneration and behavioral impairment. Whether lycopene can counteract these detrimental neurochemical and histopathological changes remains to be further verified. Objective This study investigated the effect of lycopene on cisplatin-related neurotoxicity and cognitive deficits in a rat model. Methods Thirty male Sprague‑Dawley rats were randomly assigned to five groups (n = 6 per group): control, CP‑treated, LP‑treated, CP+LP (post‑CP LP intervention), and LP+CP (LP pre‑treatment prior to CP challenge). The experiment lasted 28 days with all agents administered intraperitoneally (i.p.). The open‑field test was performed to evaluate locomotor and exploratory behaviors. Biomarkers including malondialdehyde (MDA), nitric oxide (NO), peroxynitrite (PNI), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), acetylcholinesterase (AChE), monoamine neurotransmitters (norepinephrine (NE), dopamine (DA), serotonin (5‑HT)), γ‑aminobutyric acid (GABA), glutamate dehydrogenase (GDH), ion‑dependent ATPase activities, as well as cerebellar histopathology were assessed. Results CP exposure impaired locomotor‑exploratory activity, elevated GDH, 5‑HT, MDA, NO and PNI levels, while decreasing AChE, NE, DA, GABA, ATPase activities, as well as antioxidant parameters (SOD, CAT, GPx and GSH). These changes indicated oxidative/nitrosative stress and histopathological cerebellar neurodegeneration. LP intervention normalized aberrant levels of GABA, 5‑HT, AChE, NE and DA, and preserved cerebellar histoarchitecture. Lycopene reduced MDA, NO, PNI and glutamate concentrations and restored antioxidant enzyme activities. Conclusion The findings suggest LP rescues CP-induced neurotoxicity, positioning it as a promising candidate for adjunctive therapy to alleviate CP neurotoxicity.

ABSTRACTObjectives: This research aimed to unravel the ameliorative potential of vanillic acid (VA) on lead acetate (LA)-induced cortico-hippocampal neurodegeneration in Wistar rats. Methods: Forty (40) male Wistar rats (150-180 g) were randomized into four groups (A-D) (n = 10). LA and VA were freshly prepared daily for administration in dosages based on body weight (BW). Group A was administered normal saline as control; Group B received 200 mg/kg BW of LA; Group C 200 mg/kg BW of VA and 200 mg/kg BW of LA; Group D received 200 mg/kg BW of VA. The doses were selected based on existing protocols and sample size meeting the minimum estimate by power analysis. All administration was via a single daily oral dose for 45 consecutive days. Cognitive function tests including Y-maze and open field test were done. The rats were euthanized at the end of the treatment by cervical dislocation (n = 6, per group) and ketamine anesthesia + perfusion (n = 4 per group). The brains were dissected and processed for histological, biochemical, and immunohistochemistry studies. Results: Our results revealed learning and memory deficits and neuropathological changes, such as decreased neuronal cell size and the disorganization of the neuronal network within the cortex and hippocampus of LA-induced rats, when compared to the control group. However, VA had protective function by attenuating neuronal degeneration, alleviation of cognitive deficit, and aided neuroprotection of pyramidal cells and astrocytes when compared to the LA-induced rats. Discussion: VA shows protective effects against LA-induced neurodegeneration and cognitive impairment suggesting a therapeutic role in heavy metal neurotoxicity.

Background Tramadol hydrochloride (TRM) is widely used to manage moderate to severe pain, but higher doses may cause adverse effects like cerebellar neurotoxicity. Sinapic acid (SA) is a natural phenolic acid with a strong antioxidant capacity and a promising candidate for preventing and treating neuronal injury. Objective This study focused on the effect of SA in excessive TRM exposure-induced cerebellar neurotoxicity. Method Thirty five rats were randomized into five groups (n =7): control (normal saline), TRM (50 mg/kg), SA (40 mg/kg), TRM+SA (post-treatment), and SA+TRM (pre-treatment), with daily intraperitoneal administration for 28 days. Cognitive function was assessed via the novel-object recognition and Y-maze tests. Cerebellar tissues were analyzed for its histopathological changes by Hematoxylin and Eosin (H&E) staining, as well as the levels of oxidative stress markers (Malondialdehyde (MDA) and nitric oxide (NO)), antioxidant enzymes (reduced glutathione (GSH), glutathione peroxidase (GPX) and superoxide dismutase (SOD)), inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear-related factor 2 (Nrf-2), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6) and interleukin-1 (IL-1)), neurotransmitters (acetylcholinesterase (AChE), norepinephrine (NE), dopamine (DA), serotonin (5-HT) and glutamate-dehydrogenase (GDH)), apoptotic markers (Caspase-3 and B-cell lymphoma (Bcl-2)) by biochemical assays. Results TRM exposure impaired spatial and non-spatial memory, reduced body/brain weight, and induced cerebellar damage, marked by increased oxidative stress (MDA, NO), pro-inflammatory cytokines, AChE activity, and apoptotic markers (Caspase-3), alongside decreased antioxidant enzyme activity and neurotransmitter levels (NE, DA, 5-HT, GDH). Histology revealed degenerative changes in Purkinje cells and cortical layers. SA treatment (pre- and post-) significantly ameliorated cognitive deficits, restored body/brain weight, reduced oxidative stress and inflammation, normalized antioxidant and neurotransmitter profiles, and attenuated apoptosis. Histopathological analysis showed regeneration of Purkinje cells and improved cerebellar architecture in SA-treated groups. Conclusion Sinapic acid exerts significant neuro-therapeutic effects against TRM-induced neurotoxicity via oxidative stress inhibition and down-regulation of inflammatory and apoptotic markers.

Aims: Alzheimer’s disease is a neurodegenerative disease characterized by deficiency in memory and cognition coupled with neuron loss. Previous studies reported that resveratrol is renowned for its pleiotropic effects and diverse health benefits to mankind especially in reversal of neurodegenerative disorders. The study is tailored towards investigating the ameliorative role of Resveratrol in Alzheimer’s disease (AD) pathology. Methodology: Forty (40) adult male Wistar rats (150±20g) were divided into four groups (n=10) and Drug administration spanned for a 45 days period. Group A served as the placebo to which normal saline only was administered, Group B served as the negative control group and received 200mg/kgbw of AlCl3 only, Group C received a combination of 200mg/kgbw of AlCl3 and 50mg/kgbw of resveratrol and Group D received 50mg/kgbw of resveratrol only. All animals were subjected to Neurobehavioral tests (Morris Water Maze and Y-Maze). At the end of the experiment, all animals were sacrificed and organs were harvested. Results: Biochemical estimations of antioxidant levels (GSH, CAT and SOD), stress markers (MDA), Monoamine neurotransmitters (dopamine, serotonin and norepinephrine) and histomorphology were done. Results showed that AlCl3 administration brought about a decrease in antioxidant enzyme levels and neurotransmitters (except norepinephrine) while resveratrol countered these effects (P=.05). Oxidative stress marker levels were however elevated by AlCl3 administration while resveratrol initiated a decrease (P=.05). Neuro-behavioural assessments such as Morris water maze and Y maze test indicated a decline in long-term and short-term memory due to AlCl3 administration while resveratrol served to improve these functions (P=.05). Conclusion: These results confirmed that potent capacity of resveratrol in reversing neurodegeneration in a wistar rat model of Alzheimer disease due to its antioxidant properties. Given its well documented presence in dietary sources such grapes etc, and its recognized antioxidant benefits, these findings suggest its potential as a neuroprotective agent in humans. Further translational research, including clinical trials is necessary to explore its efficacy, optimal dosage and long-term effects in Alzheimer’s disease management.

•Estradiol valerate induced PCOS in female rats and changedlipid profile,blood glucoseandgonadotropins.•Sulphoraphane improved hormonal levels and lipid profile in PCOS rats.•Sulphoraphane amended ovarian damage and improved histological changes in PCOS rats.

Cisplatin (CP) has been used in clinical oncology but causes spermatogenesis damage. Isothiocyanato-4-methylsulfonylbutane (SFN) is a potent dietary bioactive agent that has been extensively studied for its effects on disease prevention. This study focused on the intervention of SFN on Germ cell apoptosis in CP-induced testicular toxicity and sperm DNA fragmentation (SDF). A total of ninety (90) male and ninety (90) female rats (weighing, 150-200 g, 12-14 weeks old) were assigned randomly into nine groups of ten (n = 10) rats each. Group A received normal saline, group B received a single dose of 10 mg/kg CP (i.p.), group C received 50 mg/kg bwt of SFN, group D received 100 mg/kg bwt of SFN, group E received 10 mg/kg bwt CP and 50 mg/kg bwt of SFN, group F received 10 mg/kg bwt CP and 100 mg/kg bwt of SFN, group G received 10 mg/kg bwt CP and 50 mg/kg bwt vitamin C, group H received 50 mg/kg bwt of SFN and 10 mg/kg bwt CP, Group I received 100 mg/kg bwt of SFN and 10 mg/kg bwt CP. The procedure lasted for 56 days. At the end of each treatment, the 90 male rats were introduced to the 90 female rats on the proestrus at a ratio of 1:1 for fertility tests. Testicular histopathological, apoptotic marker, immunoreactivity, sperm parameters, and SDF were investigated. Cisplatin significantly decreases chromatin condensation/de-condensation levels, haploid germ cells, the number of fetuses, and BCL-2 expression. Also, CP increases SDF and BAX expression relative to control. Treatment with SFN increased BCL-2 expression, haploid germ cells, protected sperm chromatin condensation, improved microarchitecture of testes, and decreased SDF and BAX expression. Therefore, SFN protects against CP-induced apoptosis by controlling BCL-2 and BAX expression and ameliorates SDF.

Cisplatin (CP) is a highly effective antitumor agent, but its clinical use is limited due to critical adverse reactions including neurotoxicity. Quercetin (QC) is a naturally occurring phytochemical with promising bioactive effects. This study investigated the Neuroprotective mechanisms and ameliorative activities of quercetin in cisplatin-induced cerebellum neurotoxicity in rat models.The rats were randomly divided into five groups of six (n = 6) rats. Group A, served as control. Group B, received a single dose of 10 mg/kg body weight (bwt) of CP (i.p.) on the first day. Group C received 30 mg/kg bwt of QC. Group D received a single dose of 10 mg/kg bwt CP on the first day followed by 30 mg/kg bwt of QC. Group E received 30 mg/kg bwt of QC per day followed by a single dose of 10 mg/kg bwt of CP on the last day. The treatment lasted for 35 days after which the novel-object recognition memory test (NORT) was used to assess non-spatial memory function. Brain neurochemical status was assessed and brain tissues were processed for histology.Quercetin increased weight loss and cognitive performance in CP-treated rats by enhancing the exploration of unfamiliar objects. Quercetin protects the brain from CP-mediated alterations in oxidative status, as well as brain metabolic enzyme indicators. It also decreased IL-6, IL-1, and TNF-α, and NF-ĸB expression, restored brain metabolic enzyme activities, increased neurotransmitters, and prevented neuromorphological alterations.In conclusion, quercetin protects rats’ brains against CP-induced cerebellum neurotoxicity via oxidative stress inhibition and down-regulation of inflammation.

Aims: Neurodegenerative diseases pose a serious threat to public health. Manganese (Mn) is a metal necessary for biological systems; however, it can become hazardous at high concentrations, causing neurological damage. This study explores tamoxifen's potential to protect against Mn-induced neurotoxicity in adult male Wistar rats. Methodology: Forty (40) adult male Wistar Rats weighing between 170g-220g were used and divided into four groups (A-D) (n=10). Manganese (Mn) and Tamoxifen (TMX) dosages were prepared and administered daily for 45 days through oral gavage. Group A received normal saline as a placebo; Group B received 200 mg/kgbwt of Mn only; Group C received 100 mg/kgbwt of TMX and 200 mg/kgbwt of Mn; Group D received 100 mg/kgbwt of TMX only. At the end of the experiment, behavioral tests were carried out, and animals were sacrificed; the brain was then excised, cleaned, and washed with saline for analysis. Results: After the 45 days of treatment the Mn-only group exhibited clear signs of neurobehavioral toxicity. On the other hand, the TMX-treated rats exhibited significantly improved exploratory behavior and locomotor activity indicating its effect in reverting Mn neurotoxicity. The histological assessments further revealed that TMX preserved hippocampal morphology, reducing glial cell distortion and vacuolation caused by Mn exposure, while the immunohistochemical analysis showed activated Nrf-2 expression in TMX-treated groups. Conclusion: These results suggest that TMX has significant neuroprotective effects and could be a potential therapeutic agent for neurodegenerative diseases.

Polycystic ovarian syndrome (PCOS) is characterized by anovulation and hyperandrogenism symptoms. Caffeine is popularly consumed and it is a legal psychoactive substance. This study evaluated the effect of excessive caffeine intake on utero-ovarian tissue in polycystic ovary syndrome rats. Twenty-four female rats randomized into group A control received 2 ml of normal saline. Group B received 4 mg/kg body weight (bwt) i.p of estradiol valerate (EV) on the first day, Group C received 100 mg/kg bwt of caffeine orally, and Group D received i.p 4 mg/kg bwt EV and 100 mg/kg bwt of caffeine orally. The experiment lasted 30 days. Histology of the ovary and uterus, oxidative and antioxidant, reproductive hormone, lipid profile, inflammatory markers, and apoptosis markers were evaluated.The ovarian histoarchitecture revealed degeneration of the theca cells, granulosa, and corpus luteum, and loss of mucin granules in the uterine tissues in PCOS, CAF, and PCO+CAF. The estrous cycle became irregular, with prolonged diestrous and proestrus phases. Marked rise in oxidative markers and decline in the activities of ovarian enzymatic antioxidants, inflammatory response, caspase-dependent apoptosis, and hormonal imbalance.Excessive caffeine consumption, therefore impaired utero-ovarian integrity, hormones, inflammatory indicators, oxidant and antioxidant parameters, apoptotic markers, and the estrous cycle.

The potential of biomechanics for improving human health and performance is well established in many parts of the world. However, across most of Africa, biomechanics remains relatively underdeveloped. The discussion around biomechanics in the continent has increased in recent times and young African scientists are pursuing career opportunities in biomechanics-related fields within Africa and in other parts of the world. New institutions and programmes that focus on biomechanics teaching and research are also starting up around the continent. The advent of the National Biomechanics Day event, formation of the first formal biomechanics society in South Africa, along with many collaborations with relevant stakeholder organizations around the world underpin the expansion of biomechanics in Africa. This article aims to summarize the current state and describe aspirations for the future of biomechanics in Africa.

Aims: The possible toxic impact of aqueous extract of maize husks (HA) on Wistar albino rats was investigated. Study Design: Experimental design. Place and Duration of Study: This study was conducted at the Federal University of Technology, Akure, Nigeria between January 2020 and April 2020. Methodology: The extract was prepared adopting the cold extraction procedure. Forty-eight (48) Wistar albino rats were used for this study. Acute toxicity study was carried out by administering HA at a single dose of 2000, 4000 and 8000 mg/kg body weight to the rats by oral gavage. The rats were observed for 14 days for any mortality or signs of toxicity. For sub-acute study, doses of 200, 400 and 800 mg/kg body weight were orally administered daily for 28 days. Biochemical and haematological parameters as well as histopathological studies were carried out after the experiments. Results: Acute toxicity results indicated that the median lethal dose (LD50) of HA was greater than 8000 mg/kg. There was remarkable body weight gain (P ≤ 0.05) in both male and female rats in all the sub-acute groups and acute group treated with 8000mg/kg. In the acute and sub-acute toxicity study, slight difference was recorded between the biochemical and haematological parameters of the treated rats dosed with the extract and the control. There was a significant increase in Packed Cell Volume (PCV) of female rats and lymphocytes of male rats treated with 800 mg/mL and 400 mg/mL respectively. The total protein, glucose and urea level of male rats treated with 200 mg/mL reduced while urea level of females treated with 200 mg/mL and 400 mg/mL also reduced remarkably. However, histological data showed no significant difference. Conclusion: In general, the extract was found to show no toxic effect on the rats and hence it is safe for potential therapeutic use.

•Cisplatin (CP) induced testicular dysfunctions.•CP-induced seminiferous epithelium degeneration.•1-isothiocyanate-4-methyl sulfonyl butane (SFN) increased sperm quality.•SFN maintain testicular integrity.•SFN enhances spermatogenesis.

•Excessive exposure to tramadol induced hepatorenal toxicity.•Vitamin B12 is an essential water-soluble vitamin, commonly found in a variety of foods.•Vitamin B12 maintain liver and kidney integrity.•Vitamin B12 supplementation ameliorate hepatorenal damage.

Graphical Abstract Abstract Background This study aims to study the histomorphological response of d-ribose-l-cysteine (DRLC) to ketamine-induced testicular damage in adult male Wistar rats. Methods A total of 20 adult male Wistar rats were used for this experiment. The animals were randomly divided into four groups (A–D) (n = 5). Group A served as the control, receiving distilled water as placebo; animals in group B were administered with 50 mg/kg body weight (bw) of ketamine only; animals in group C were administered with 50 mg/kg bw of ketamine and 30 mg/kg bw of DRLC; animals in group D were administered with 30 mg/kg bw of DRLC only. At the end of the experiment, blood was taken from the heart via cardiac puncture and stored, semen was collected from the caudal epididymis for immediate sperm analysis, while the testes were excised and preserved for histological examination and biochemical analysis. Results The results showed abnormalities marked by a significant decrease in the weights, sperm parameters, as well as antioxidants, serum hormonal levels and abnormal testicular microarchitecture in the rats as a result of ketamine treatment. However, DRLC exhibits significant quenching effects and attenuating activities on the ketamine-induced abnormalities by increasing the rats' weights, restoring the sperm parameters, as well as increasing the antioxidants and serum hormonal levels with restored testicular histoarchitecture. Conclusion DRLC in the current study attenuated the toxic effects of ketamine on the testes; therefore, it could be used as adjuvant therapy for reproductive toxicant-induced testicular toxicity due to its potent antioxidant property. Significance statement The testis is a vital secreting organ that produces and stores spermatozoa and is crucial for producing male sexual hormones and is thus the main target of infertility when overdoses of chemicals and toxins are introduced to it. In view of the facts above, studies of the potential of chemicals like ketamine to induce testicular toxicity are important as well as the methods aimed at mitigating this effect. Various studies have been conducted on the effectiveness of DRLC in subsiding different chronic health conditions, but there is no published literature on the effects of DRLC in ketamine-induced testicular toxicity in adult male Wistar rats. Hence we present this study.

Zinc (Zn) has proven to play a key role in spermatogenesis. The present study focused on the nutritional supplementation of Zn against cisplatin (CP)-induced spermatogonial and testicular dysfunctions. Thirty-two (32) mature male Sprague Dawley rats were randomized into four groups of eight (n = 8) rats each – Control group (received 2 ml of normal saline); Zn group (received 1 mg/kg body weight (bwt) of Zn sulfate); Cisplatin group treated intraperitoneally with a single dose (10 mg/kg bwt) of CP; and CP + Zn group, after induction of testicular toxicity, were treated (orally) with 1 mg/kg bwt of Zn sulfate. The procedure lasted for 8 weeks. Parameters tested include testicular histology, sperm parameters, testosterone (TT), follicle-stimulating hormone (FSH) and luteinizing hormone (LH), catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione reductase (GR), thiobarbituric acid reactive substances (TBARS). Cisplatin significantly decreases (p < 0.05) sperm quality, testosterone, FSH and LH, epithelial cell height, tubular diameter, number of spermatogonia, spermatocytes, and spermatids with concomitant increase in thiobarbituric acid reactive substances (TBARS). Zinc supplementation reversed the toxic effect of CP on sperm characterization, hormone profiling, histological and biochemical parameters. Zinc supplementation, therefore, ameliorates the deleterious effect of CP on cytoarchitecture of the testis, protected the seminiferous epithelium, and reduced oxidative stress thereby promoting spermatogenesis.

Lead is a common environmental toxicant associated greatly with hematological and hormonal imbalance, biochemical alterations, and reproductive abnormalities. This study was conducted to evaluate the effects of D-ribose-L-cysteine (DRLC) on hematobiochemical and reproductive toxicity associated with lead acetate exposure in adult female Wistar rats. Thirty-two adult female Wistar rats (165 +/- 20 g) were divided into four groups (n = 8). Group A received normal saline as placebo; Group B received 100 mg/kg BW of lead acetate only; Group C received 100 mg/kg BW of lead acetate and 10 mg/kg BW DRLC (low dose); Group D received 100 mg/kg BW of lead acetate and 30 mg/kg BW of DRLC (high dose). All administration was done via oral gavage for 42 days, thereafter animals were sacrificed; serum was obtained from the blood collected for analysis, ovaries, and uterus was harvested for analysis. The lead acetate only group showed a significant difference in hematological indices relative to control. Additionally, there was a significant decrease in body weight, sodium dismutase, catalase, reduced glutathione, progesterone with a corresponding increase in ovarian weight, MDA, FSH, and LH among the lead acetate only group relative to the control. Histological observation showed atretic antral follicles, with detached granulosa cells, pyknotic nuclei in the granulosa wall in the ovaries of the lead-exposed only group compared to the control. Co-administration of DRLC and lead attenuate the toxicity of lead exposure by restoring the hematological values, biochemical parameters, hormone profile, and morphology of the ovary. Exposure to lead acetate causes deleterious toxicity to hematological and reproductive functions which were ameliorated DRLC supplementation through its antioxidant mechanisms.

BACKGROUND:Classroom furniture designs have been implicated in musculoskeletal disorders among school age persons due to high level mismatches between the furniture dimensions and users' anthropometrics.OBJECTIVE:The objective of the study was to analyze classroom furniture ergonomics at selected primary, secondary and tertiary educational institutions in Nigeria and to understand if there are noticeable patterns in the match/mismatch.METHOD:Anthropometric measures relevant to furniture design were obtained from primary and secondary school children as well as from university undergraduates. The dimensions of classroom furniture available to the participants were also taken and an assessment of the suitability of the furniture was completed.RESULT:The ergonomic evaluation of the classroom furniture available to the study participants revealed enormous discrepancies between the furniture dimensions and the anthropometric measures of the users. In addition, a pattern was observed in the way the matches/mismatches occurred. The furniture dimensions that matched majority of the users tend to match across the three categories and those that did not match majority of the students, also followed the same pattern.CONCLUSION:The study presents remarkably high levels of mismatches between classroom furniture and users' anthropometrics and therefore calls for a review of the policies for classroom furniture design in Nigeria, if at all any policy exists.

Graphical abstract Abstract Di-2-ethylhexyl phthalate (DEHP) is an extensively used plasticizer which has raised some concerns about its safety on human health. This study aimed at evaluating the effects of vanillic acid (VA) and vitamin C (VC) supplementation on DEHP-induced testicular toxicity. Thirty-five adult male Wistar rats were randomly divided into 7 groups (A–G) ( n = 5 ) receiving distilled water; 250 mg/kg bw of DEHP only; 30 mg/kg bw of VA and 250 mg/kg bw of DEHP; 30 mg/kg bw of VC and 250 mg/kg bw of DEHP; 30 mg/kg bw of DEHP plus 30 mg/kg bw of VA and 30 mg/kg bw of VC; 30 mg/kg bw of VA only; and 30 mg/kg bw of VC only, respectively. At the end of the experiment, blood was taken from the heart via cardiac puncture and stored, semen was collected from the caudal epididymis for immediate sperm analysis, while the testes were excised and preserved for histological examination and biochemical analysis. The results showed a significant decrease ( P < 0.05) in body weights, sperm motility, sperm volume, sperm viability and count, antioxidant levels, and reproductive hormonal levels, with a significant increase ( P < 0.05) in sperm morphological defect and lipid peroxidation level in DEHP-only group compared with the control but was ameliorated after VA and VC administration compared to the DEHP-only treated animals. VA and VC supplementation attenuated the toxic effects of DEHP on the testicular functions, morphology, and semen characterization of the experimental adult male Wistar rats. Lay summary Male infertility is considered when identifiable female causes of infertility are excluded and semen quantity and quality fail to fulfil World Health Organization criteria. From conception through to adulthood, people are exposed to limitless environmental toxicants among which di-2-ethylhexyl phthalate (DEHP) commonly found in personal care products, cosmetics, and medical devices is prevalent. The present study elaborated on the importance of taking antioxidant-rich foods containing vitamin C and vanillic acid, such as those found in various fruits, olives, whole wheat, and cereal grains, in combating infertility caused by environmental toxicants. An experiment was carried out on rats to see the effect of vanillic acid and vitamin C supplementation on preventing DEHP-induced testicular toxicity. The testicles and semen were analyzed from five rats in each treated and control groups. The data led us to conclude that vanillic acid and vitamin C supplementation do have attenuating effects on DEHP-induced testicular toxicity, due to their high antioxidant and anti-inflammatory properties.

Diabetes mellitus (DM) is one of the leading causes of death globally and complications of DM have become a major health concern. Anacardium occidentale is a plant widely recognized for its hypoglycemic properties and traditionally used in developing nations as remedy for DM treatment. Riboceine is a supplement that enhances production of glutathione and known for its vital role in supporting cellular function. This study was designed to evaluate the antidiabetic and antioxidant potential of riboceine and ethanolic extract of A. occidentale leaves in streptozotocin (STZ)-induced diabetic rats. Twenty-nine adult male Wistar rats were induced with DM intraperitoneally using a single dose of STZ (70 mg/kg). The STZ-induced rats were divided into groups and administered the same dose (100 mg/kg) of A. occidentale leaves extract and riboceine via gastric gavage at the dose (100 mg/kg) for seventeen days while metformin (40 mg/kg) was used as positive control. Fasting blood glucose and weight of the model rats were examined periodically. Activities of total protein, creatinine, urea, antioxidants (SOD, GSH and GPX), and level of serum insulin were determined. Expression of diabetes related genes including pancreas (Insulin, pdx-1, P16NK4A, and Mki-67), Liver (FAS, ACC, and GFAT) and KIM-1 genes were also determined. Data showed that treatment of STZ-induced diabetic rats with A. occidentale and riboceine at the same dose significantly (p < 0.05) ameliorated hyperglycemic effects by improving hepatic and renal functions and antioxidants, preventing hepatic fat accumulation by downregulation of ACC, FAS and GFAT expression, improving β-cell functions through up-regulation of pancreatic insulin, P16NK4A, Mki-67 and pdx-1 expression. Induction of diabetes upregulated mRNA expression of KIM-1, which was ameliorated after treatment of the rats with A. occidentale and riboceine. The results obtained in this study demonstrate significant antidiabetic properties of ethanolic extract of A. occidentale and riboceine.