The exposure to blue and white Light emitting diodes (LED) light leads to damage in the visual system with short-term LED light exposure. Chronic exposure, adaptive responses to light, and self-protective mechanisms against LED light exposures need to be explored, and it would be essential to understand the repercussions of LED radiation on vitreous metabolites. A total of 24 male Wistar rats were used in this study, divided into four groups (n = 6 in each group). Three experimental groups of rats were exposed to either blue, white, or yellow LED light for 90 days (12:12 light-dark cycle routine) with uniform illumination (450–500 lux). Standard lab settings were used to maintain control rats. Vitreous fluids were subjected to untargeted metabolomics analysis using liquid chromatography-mass spectrometry (LC/MS). PLS-DA analysis indicated significant the separation of m metabolites among groups, suggesting that LED exposure induces metabolic reprogramming in the vitreous. Amino acids and their modifications showed significant alterations among groups which included D-alanine, D-serine (p < 0.05), lysine (p < 0.001), aspartate (p = 0.0068), glutathione (p = 0.0263), taurine (p = 0.007), and hypotaurine. In chronic light exposure, the self-protective or reworking system could be depleted, which may decrease the ability to compensate for the defending mechanism. This might fail to maintain the metabolomic structural integrity of the vitreous metabolites.

Nutrition plays a critical role in the brain's function and development. Vitamin B6 in the form of pyridoxal phosphate (PLP) is required for the biosynthesis of several neurotransmitters. As vitamin B6 is not endogenously synthesized, the availability of dietary sources becomes imperative. Due to its contribution to neurological functions, severe vitamin B6 deficiency leads to an increased risk of psychiatric disorders, dementia, and neurodevelopmental disorders. This study aimed to establish a vitamin B6-deficient model in experimental animals and assess the neurodevelopmental effects in their offspring. Two- to three-month-old female C57BL/6J mice were used in the study. They were randomly divided into control and vitamin B6-deficient groups. The control group was fed a regular diet containing 6 mg vitamin B6/kg and the vitamin B6-deficient group was fed a customized diet containing 0 mg vitamin B6/kg, for 5 weeks (n = 6). After 5 weeks, plasma PLP was assessed. The animals were bred to generate offspring. The dams were killed following weaning, and the hippocampal neurons were quantified using cresyl violet staining. The offspring were assigned the respective diet post-weaning up to 2 months of age. Learning and memory were assessed using the Morris water maze test. The plasma PLP levels confirmed the deficiency in the deficient group compared to the control group. The viable pyramidal neurons in the cornu ammonis 3 (CA3) region of the hippocampus showed a significant difference between the control and deficient groups. Offspring born to deficient dams showed a substantial increase in latency to reach the target quadrant during the probe trial compared to the controls. Vitamin B6 deficiency reduces memory in dams and their offspring, suggesting the importance of vitamin B6 for both brain function and development.

Background and Aim: Cisplatin (CP) is a preferred drug for cancer treatment but it has dose-dependent side effects. Vitex agnus-castus (VAC) berry extract has antioxidant, free-radical scavenging, and anti-inflammatory activities. This study explored the mitigating effects of VAC extract (VACE) on acute hematotoxicity induced by CP in female Wistar rats. Materials and Methods: Female Wistar rats (n = 30) were randomly divided into five groups (n = 6/group). The normal control (NC) group received no treatment. The CP control group received CP (7 mg/kg.b.w. ip, single dose) and the drug control group (VACE-650) received VACE (650 mg/kg b.w. oral, daily) for 7 days. Both groups received a single dose of CP (7 mg/kg b.w. ip), followed by 350 and 650 mg/kg.b.w. of VACE daily orally (CPVACE-350 and CPVACE-650 groups, respectively) for 7 days. Results: After a single dose of CP (7 mg/kg b.w.), the red blood cells (RBC), hematocrit (HCT), white blood cells (WBC), and platelets significantly decreased. In the VAC-350 group, the reduction in total WBC count was less than that in the VAC-650 group on the 3rd day. The RBC and HCT values of the VACE groups were better than that of the CP control, but the VACE-350 treatment group showed significant improvement only on the 3rd day. Conclusion: Our findings showed that VACE can mitigate CP-induced damage to peripheral blood cells at lower doses. Keywords: cisplatin, hematotoxicity, rats, Vitex agnus-castus.

Background: Cisplatin (CP) is used to treat various solid tumors but is associated with nephrotoxicity, which varies with dose and duration. Vitex Agnus castus (VAC) berries, known for their anti-inflammatory and antioxidant properties, may alleviate CP-induced renal toxicity. Objective: To investigate the gender-specific responses to cisplatin-induced nephrotoxicity and evaluate VAC extract's nephroprotective effects. Methods: Four-month-old Wistar rats (n=36) (24 male, 12 female) were used. In phase 1, gender-based differences in CP-induced nephrotoxicity were assessed. The gender group with higher nephrotoxicity was selected for phase 2 to evaluate VAC's nephroprotective properties. Animals were randomly grouped as Normal Control (6 males & 6 females), CP Control (6 males & 6 females) received CP (7 mg/kg bw) injection, VAC Control (received 165 mg/kg bw VAC for 7 days daily), and CP+VAC (CP injection followed by VAC orally for 7 days). Results: CP-treated male rats showed significantly higher plasma creatinine, urea, and BUN levels (p<0.05) than controls, while female rats showed slight increases. Male rats were chosen for phase 2, where VAC treatment post-CP injection lowered the kidney function parameters, though not significantly compared to CP controls. Histopathology revealed severe tubular damage and dilation in CP-treated kidneys compared to controls. Conclusion: Cisplatin (7 mg/kg bw) causes acute kidney injury, with male rats showing more nephrotoxicity. VAC extract reduced biochemical markers of nephrotoxicity but did not reverse CP-induced damage, suggesting potential mitigation of some CP-induced renal toxicity.