**Background:** The depletion of the ozone layer has increased human exposure to ultraviolet radiation (UVR), which is known to cause skin cancers, cataracts, and immune system damage. However, moderate UVR exposure can increase vitamin D activity, important for calcium metabolism and immunity. During pregnancy, maternal environmental exposures can influence fetal development and later health. This study aimed to investigate markers of immune and inflammatory responses in offspring of pregnant Wistar rats exposed to UVR at different gestational stages.
**Methods:** Thirty pregnant Wistar rats (100-120 g) were divided into six groups (n=5 each). Group I (control) was not exposed to UVR. Groups II, III, IV, V, and VI were exposed daily for one hour to UVA (350 nm), UVB (312 nm), and UVC (254 nm) on gestational days 1-7, 8-14, 15-21, 1-14, and 1-21, respectively. Offspring birth weight was recorded, and on postnatal day 10, body weight was measured. Blood samples were collected via cardiac puncture under diethyl ether anesthesia and analyzed for total protein, albumin, globulin, C-reactive protein (CRP), interleukin-1β (IL-1β), and complement component C3 using ELISA kits. Liver samples were examined histologically with hematoxylin and eosin stains. Data were expressed as mean ± SEM, and statistical differences were evaluated using ANOVA and Mann-Whitney U post-hoc test, with significance at p<0.05.
**Key Results:** Offspring birth weight was significantly increased (p<0.05) in all experimental groups compared to controls: group II (45.9%), III (57.9%), IV (43.8%), V (36.1%), and VI (48.4%). However, percent weight gain on postnatal day 10 was lower in all experimental groups (148.8%, 129.4%, 146.5%, 151.1%, and 171.1%) compared to controls (272.8%). No significant differences were observed in liver weight, total protein, or albumin levels across groups, except albumin was significantly decreased in group VI (2.66±0.05 mg/dL) vs controls (3.51±0.40 mg/dL). Globulin levels were significantly increased (p<0.05) in groups IV (3.23±0.20 mg/dL), V (2.65±0.05 mg/dL), and VI (3.42±0.44 mg/dL) compared to controls (1.81±0.11 mg/dL). CRP levels (ng/mL) were significantly elevated in groups II (1.75±0.09), IV (1.61±0.13), V (1.24±0.05), and VI (1.10±0.04) vs controls (0.89±0.07), but not in group III. IL-1β levels (pg/mL) were significantly increased in groups II (136.1%), III (91.8%), V (83.6%), and VI (216.4%) compared to controls (0.61±0.06), while group IV (0.76±0.07) was not significantly different. Complement C3 levels showed no significant differences across groups. Histological examination revealed hepatocellular degeneration and necrosis in all experimental groups, including multifocal coagulation necrosis (group II), centrilobular degeneration (group III), periportal vacuolar degeneration and inflammation (group IV), random necrosis with fibroblast proliferation (group V), and centrilobular necrosis (group VI), while controls had normal liver architecture.
**Clinical Implications:** This study demonstrates that maternal exposure to UVR during gestation can alter offspring immune and inflammatory responses, as evidenced by increased CRP and IL-1β levels, elevated globulin, and liver histopathology. The increased birth weight may be due to UVR-induced vitamin D synthesis, but the reduced postnatal weight gain and inflammatory markers suggest potential adverse effects on neonatal health. The findings indicate that gestational UVR exposure may activate maternal proinflammatory mediators that are transferred to the fetus, modulating the innate immune system. This has implications for understanding how environmental UVR exposure, especially with ozone depletion, might affect fetal programming and later disease susceptibility. However, the study did not isolate the effects of individual UVR types, and further research is needed to clarify mechanisms and assess long-term outcomes.