Ultraviolet (UV) radiation, comprising UVA and UVB rays, poses a significant threat to human health. This review aims to elucidate the differences between UVA and UVB radiation in their ability to induce DNA damage, shedding light on the underlying molecular mechanisms involved. Understanding these mechanisms is crucial for developing strategies to mitigate the harmful effects of UV radiation. The study analyzed histological changes in UVA and UVB-exposed skin and explored matrix metalloproteinases (MMPs) and reactive oxygen species (ROS) in UV-induced skin damage. It examined DNA lesions caused by UVA and UVB radiation. UVA radiation led to dermal integrity loss, collagen breakdown, and inflammatory infiltration, while UVB radiation primarily resulted in keratinocyte proliferation. UVA-induced MMP activation accelerated collagen breakdown, whereas UVB exposure moderately increased MMP activity. UVA caused more DNA and protein oxidation, while UVB primarily induced oxidative protein modification and endoplasmic reticulum (ER) stress. UVA-induced oxidative stress and DNA damage were associated with skin cancer, premature aging, and immune suppression. UVB radiation directly interacted with DNA, forming cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs), which are strongly associated with skin cancer development. UVA and UVB radiation have distinct characteristics and induce different DNA lesions. Repair mechanisms, such as nucleotide excision repair (NER) and base excision repair (BER), play crucial roles in maintaining genomic integrity. Understanding the mechanisms underlying UVA and UVB-induced DNA damage and repair is essential for developing targeted prevention and therapeutic approaches to combat the harmful effects of UV radiation.